CN114085833A - miR-25-3p, application and application method thereof - Google Patents

miR-25-3p, application and application method thereof Download PDF

Info

Publication number
CN114085833A
CN114085833A CN202111329966.6A CN202111329966A CN114085833A CN 114085833 A CN114085833 A CN 114085833A CN 202111329966 A CN202111329966 A CN 202111329966A CN 114085833 A CN114085833 A CN 114085833A
Authority
CN
China
Prior art keywords
mir
growth
neurons
nerve injury
cortical
Prior art date
Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
Pending
Application number
CN202111329966.6A
Other languages
Chinese (zh)
Inventor
周松林
丁斐
从猛
张琦
沈宓
刘畅
Current Assignee (The listed assignees may be inaccurate. Google has not performed a legal analysis and makes no representation or warranty as to the accuracy of the list.)
Nantong University
Original Assignee
Nantong University
Priority date (The priority date is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the date listed.)
Filing date
Publication date
Application filed by Nantong University filed Critical Nantong University
Priority to CN202111329966.6A priority Critical patent/CN114085833A/en
Publication of CN114085833A publication Critical patent/CN114085833A/en
Pending legal-status Critical Current

Links

Images

Classifications

    • C—CHEMISTRY; METALLURGY
    • C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
    • C12N—MICROORGANISMS OR ENZYMES; COMPOSITIONS THEREOF; PROPAGATING, PRESERVING, OR MAINTAINING MICROORGANISMS; MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA
    • C12N15/00—Mutation or genetic engineering; DNA or RNA concerning genetic engineering, vectors, e.g. plasmids, or their isolation, preparation or purification; Use of hosts therefor
    • C12N15/09—Recombinant DNA-technology
    • C12N15/11—DNA or RNA fragments; Modified forms thereof; Non-coding nucleic acids having a biological activity
    • C12N15/113—Non-coding nucleic acids modulating the expression of genes, e.g. antisense oligonucleotides; Antisense DNA or RNA; Triplex- forming oligonucleotides; Catalytic nucleic acids, e.g. ribozymes; Nucleic acids used in co-suppression or gene silencing
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
    • A61K31/00—Medicinal preparations containing organic active ingredients
    • A61K31/70—Carbohydrates; Sugars; Derivatives thereof
    • A61K31/7088—Compounds having three or more nucleosides or nucleotides
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
    • A61P25/00—Drugs for disorders of the nervous system
    • A61P25/02—Drugs for disorders of the nervous system for peripheral neuropathies
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
    • A61P25/00—Drugs for disorders of the nervous system
    • A61P25/28—Drugs for disorders of the nervous system for treating neurodegenerative disorders of the central nervous system, e.g. nootropic agents, cognition enhancers, drugs for treating Alzheimer's disease or other forms of dementia
    • C—CHEMISTRY; METALLURGY
    • C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
    • C12N—MICROORGANISMS OR ENZYMES; COMPOSITIONS THEREOF; PROPAGATING, PRESERVING, OR MAINTAINING MICROORGANISMS; MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA
    • C12N15/00—Mutation or genetic engineering; DNA or RNA concerning genetic engineering, vectors, e.g. plasmids, or their isolation, preparation or purification; Use of hosts therefor
    • C12N15/09—Recombinant DNA-technology
    • C12N15/87—Introduction of foreign genetic material using processes not otherwise provided for, e.g. co-transformation
    • C—CHEMISTRY; METALLURGY
    • C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
    • C12N—MICROORGANISMS OR ENZYMES; COMPOSITIONS THEREOF; PROPAGATING, PRESERVING, OR MAINTAINING MICROORGANISMS; MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA
    • C12N5/00—Undifferentiated human, animal or plant cells, e.g. cell lines; Tissues; Cultivation or maintenance thereof; Culture media therefor
    • C12N5/06—Animal cells or tissues; Human cells or tissues
    • C12N5/0602—Vertebrate cells
    • C12N5/0618—Cells of the nervous system
    • C12N5/0619—Neurons
    • C—CHEMISTRY; METALLURGY
    • C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
    • C12N—MICROORGANISMS OR ENZYMES; COMPOSITIONS THEREOF; PROPAGATING, PRESERVING, OR MAINTAINING MICROORGANISMS; MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA
    • C12N2320/00—Applications; Uses
    • C12N2320/30—Special therapeutic applications
    • C—CHEMISTRY; METALLURGY
    • C12—BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
    • C12N—MICROORGANISMS OR ENZYMES; COMPOSITIONS THEREOF; PROPAGATING, PRESERVING, OR MAINTAINING MICROORGANISMS; MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA
    • C12N2510/00—Genetically modified cells

Landscapes

  • Health & Medical Sciences (AREA)
  • Engineering & Computer Science (AREA)
  • Life Sciences & Earth Sciences (AREA)
  • Biomedical Technology (AREA)
  • Genetics & Genomics (AREA)
  • Chemical & Material Sciences (AREA)
  • Bioinformatics & Cheminformatics (AREA)
  • Organic Chemistry (AREA)
  • Biotechnology (AREA)
  • General Health & Medical Sciences (AREA)
  • Wood Science & Technology (AREA)
  • Zoology (AREA)
  • General Engineering & Computer Science (AREA)
  • Neurology (AREA)
  • Neurosurgery (AREA)
  • Molecular Biology (AREA)
  • Biochemistry (AREA)
  • Medicinal Chemistry (AREA)
  • Veterinary Medicine (AREA)
  • Public Health (AREA)
  • Animal Behavior & Ethology (AREA)
  • Microbiology (AREA)
  • Pharmacology & Pharmacy (AREA)
  • Chemical Kinetics & Catalysis (AREA)
  • Nuclear Medicine, Radiotherapy & Molecular Imaging (AREA)
  • General Chemical & Material Sciences (AREA)
  • Physics & Mathematics (AREA)
  • Biophysics (AREA)
  • Plant Pathology (AREA)
  • Epidemiology (AREA)
  • Cell Biology (AREA)
  • Hospice & Palliative Care (AREA)
  • Psychiatry (AREA)
  • Medicines That Contain Protein Lipid Enzymes And Other Medicines (AREA)
  • Measuring Or Testing Involving Enzymes Or Micro-Organisms (AREA)

Abstract

The invention provides miR-25-3p, an application and an application method thereof, and relates to the technical field of biomedicine, wherein the miR-25-3p is used as a molecular intervention target point to overexpress miR-25-3p so as to promote the growth of axons of DGR neurons and cortical neurons. The miR-25-3p participates in the repair of peripheral nerve injury by regulating the axonal growth of DGR neurons. The miR-25-3p participates in central nerve injury repair by regulating the growth of cortical neuron axons. According to the invention, firstly, a small RNA, namely miR-25-3p is found to play an important role in repairing nerve injury through screening. In vitro DRG neurons, miR-25-3p imic is transfected, so that the growth of primary culture DRG neurons and cortical neuron axons can be remarkably promoted. The miR-25-3p can participate in peripheral nerve injury repair by regulating the growth of DRG neuron axons, and can also participate in central nerve injury repair by regulating the growth of cortical neuron axons. The miRNA is helpful for better understanding the important role of miRNA in the nerve injury repair process, and provides a new target for treatment after nerve injury.

Description

miR-25-3p, application and application method thereof
Technical Field
The invention relates to the technical field of biomedicine, in particular to miR-25-3p, application and an application method thereof.
Background
Nerve injury repair is a common clinical problem, and causes great burden to society and families. Peripheral nerves can be spontaneously regenerated after being damaged, but the regeneration speed is limited, so that the function is difficult to recover, and meanwhile, spinal cord injury is one of destructive diseases which cause the damage of the nerve function and the reduction of the life quality, the morbidity and the mortality are high, and the economic and social burden is heavy. Therefore, the cell and molecular mechanism of nerve injury regeneration is fully explored, the nerve function repair is promoted, and a theoretical basis is provided for clinical treatment.
microRNA (miRNA) is endogenous small non-coding RNA, is about 21-23 nucleotides in length, and has the main function of inhibiting the translation of a target gene or directly degrading the target gene by completely or incompletely combining with a non-translation region at the 3' end of the target gene.
Disclosure of Invention
The invention aims to solve the technical problem that in the prior art, the regeneration speed is limited after a nerve is damaged, and finally, the function is difficult to recover.
In order to achieve the purpose, the invention adopts the following technical scheme:
miR-25-3p is used as a molecular intervention target point, and is used for over-expressing miR-25-3p to promote the growth of DGR neuron and cortical neuron axons.
The application also provides application of the miR-25-3p, wherein the miR-25-3p is involved in peripheral nerve injury repair by regulating the axonal growth of DGR neurons.
Preferably, said miR-25-3p is involved in central nerve injury repair by modulating cortical neuron axonal growth.
The application also provides an application method of the miR-25-3p, which comprises the following steps:
s1: the miR-25-3p is expressed in vitro to promote the growth of the axon of cortical neurons;
s2: in vitro miR-25-3p expression promotes DRG neuron axon growth;
s3: overexpression of miR-25-3p in vitro inhibits Pten expression in cortical neurons.
Preferably, the specific steps in S1 are:
a1: culturing primary cortical neuronal cells;
a2: transfecting neuron cells with mimics;
a3: cellular immunofluorescent stain axon growth length measurement.
Preferably, the specific steps in S2 are:
b1: culturing primary DRG neuron cells;
b2: transfecting neuron cells with mimics;
b3: cellular immunofluorescence staining and axon regeneration length measurement.
Preferably, the specific steps in S3 are:
c1: culturing primary cortical neuronal cells;
c2: transfecting neuron cells with mimics;
C3：Western blot。
miR-25-3p is used as a molecular intervention target point, the miR-25-3p is overexpressed, and the growth of DRG neuron and cortical neuron axons is promoted.
In the application, firstly, a small RNA, namely miR-25-3p is found to play an important role in repairing nerve injury through screening. In vitro DRG neurons, miR-25-3p imic is transfected, so that the growth of primary culture DRG neurons and cortical neuron axons can be remarkably promoted. The miR-25-3p can participate in peripheral nerve injury repair by regulating the growth of DRG neuron axons, and can also participate in central nerve injury repair by regulating the growth of cortical neuron axons. The miRNA is helpful for better understanding the important role of miRNA in the nerve injury repair process, and provides a new target for treatment after nerve injury.
Drawings
FIG. 1 is a schematic diagram of the in vitro overexpression of miR-25-3p according to an embodiment of the invention can significantly promote the growth of cortical neuronal axons;
FIG. 2 is a schematic diagram of the in vitro overexpression of miR-25-3p can significantly promote the growth of DRG neuronal axons according to one embodiment of the invention;
FIG. 3 is a schematic diagram that in vitro overexpression of miR-25-3p can significantly inhibit protein expression of PTEN in DRG neurons according to an embodiment of the invention.
Detailed Description
In order to make the objects, technical solutions and advantages of the present invention more apparent, the present invention is further described in detail with reference to the following embodiments.
In the following description, numerous specific details are set forth in order to provide a thorough understanding of the present invention, however, the present invention may be practiced in other ways than those specifically described herein, and thus the present invention is not limited to the specific embodiments of the present disclosure.
The application provides miR-25-3p serving as a molecular intervention target point, and the miR-25-3p is overexpressed and is used for promoting the growth of axons of DGR neurons and cortical neurons.
The application also provides an application of the miR-25-3p, which participates in peripheral nerve injury repair by regulating the growth of DGR neuron axons and participates in central nerve injury repair by regulating the growth of cortical neuron axons.
The application also provides an application method of the miR-25-3p, which comprises the following steps:
s1: in vitro overexpression of miR-25-3p for promoting growth of cortical neuron axons
Specifically, in one embodiment, the step S1 includes the following steps:
a1: culturing primary cortical neuronal cells:
specifically, in one embodiment, cortical neurons are from SD rats pregnant for 18 days, the cerebral cortex is removed and placed in the dissecting fluid HA, digested with a suitable amount of 0.25% pancreatin, and then placed at 37 ℃ for 20 min.
Pancreatin was stopped with DMEM containing 10% fetal bovine serum, and the supernatant was discarded after centrifugation.
The cells were resuspended in DMEM containing 10% FBS, passed through a 70 μm mesh screen, and the supernatant discarded by centrifugation.
10% FBS DMEM heavy suspension cells, after counting, with 5 x 104Cell number per well was plated into 24-well plates coated with polylysine.
A2: neuronal cell mimics transfection
Specifically, in one embodiment, after culturing for 4h, after the cells adhered to the wall, the cells were cultured in Lipofectamine RNAiMAX Reagent, mixed with miR-25-3p mimics, a negative control (20 nM final concentration, manufactured by Sharp Bo Bio Inc., Guangzhou), 2% B-27, 2mM glutamine Neurobasal medium, and added to the cultured neurons, and the cells were cultured for 12h and then replaced with the neuron culture medium without transfection reagents.
A3: cellular immunofluorescent stain axon growth length measurement:
specifically, in one embodiment, after 72 h after transfection of cortical neuronal cells, the cell culture medium is discarded, rinsed twice with PBS, added with 4% paraformaldehyde, and fixed for 30 min.
After discarding paraformaldehyde, the PBS was washed three times for 5 min each.
Adding immunohistochemical blocking solution, and blocking at room temperature for 1 hr.
Primary antibodies anti-Tuj1 antigen (1: 500, abcam) were diluted with immunohistochemical primary antibody diluent and added overnight at 4 ℃.
Primary antibody was discarded and washed 3 times with PBS for 5 min each.
The fluorescent secondary antibody anti-mouse 594 (1: 500, Invitrogen) was diluted with the immunohistochemical secondary antibody diluent, and after adding the secondary antibody, it was protected from light for 2h at room temperature.
The secondary antibody was discarded and washed 3 times with PBS for 5 min each time.
An appropriate amount of PBS was added, and the mixture was observed under a Leica fluorescence microscope and photographed.
And observing the growth condition of the protrusions, photographing and counting the distribution of the lengths of the protrusions in each group.
The results are shown in fig. 1, where fig. 1A is a schematic representation of the immunohistochemical staining of cells after 72 h of in vitro cultured cortical neurons transfected with either mic Negative control (mic-NC, Negative control) or miR-25-3 pmimics respectively, as used herein, and fig. 1B is the average length of cortical neuron axon growth under Bar =75 μm, P < 0.01, as can be seen: the miR-25-3p (miR-25-3 p mimics) is overexpressed, so that the growth of cortical neuron axons can be remarkably promoted.
S2: in vitro overexpression of miR-25-3p for promoting growth of DRG neuron axons
B1: culturing primary DRG neuronal cells
DRG neurons were from the red skin of 1 d-SD rats, dorsal root ganglia were removed and placed in dissecting fluid HA, digested with appropriate amount of 3 mg/ml collagenase, at 37 deg.C for 30 min. Discarding collagenase, adding appropriate amount of 0.25% pancreatin for digestion at 37 deg.C for 20 min. Pancreatin was stopped with DMEM containing 10% fetal bovine serum, and the supernatant was discarded after centrifugation. Cells were resuspended in Neurobasal media with 2% B-27 and 2mM glutamine and sieved through a 70 μm sieve. After centrifugation, the supernatant was discarded, the cells were resuspended in 5ml of 10% BSA, and the supernatant was discarded by centrifugation. The cells were resuspended in 1ml of 2% B-27 and 2mM glutamine in Neurobasal medium and counted.
B2: neuronal cell mimics transfection
After the cells are counted, cell suspension with the concentration of 2 × 104/hole, Lipofectamine RNAiMAX Reagent, miR-25-3p mimics and negative control (20 nM final concentration, Yangzhou Ruibo biology company) are uniformly mixed and then added into cultured neurons, the neurons are planted into a 24-hole plate coated with polylysine, and the neuron culture medium containing 10mM cytarabine is replaced after 12h culture for removing non-neuronal cells.
B3: cellular immunofluorescent staining and axon regeneration length measurement
DRG neuron cells were transfected for 72 h, rinsed twice with PBS, added with 4% paraformaldehyde, and fixed for 30 min.
After discarding paraformaldehyde, the PBS was washed three times for 5 min each.
Adding immunohistochemical blocking solution, and blocking at room temperature for 1 hr.
Primary antibodies anti-Tuj1 antigen (1: 500, abcam) were diluted with immunohistochemical primary antibody diluent and added overnight at 4 ℃.
Primary antibody was discarded and washed 3 times with PBS for 5 min each.
The fluorescent secondary antibody anti-mouse 594 (1: 500, Invitrogen) was diluted with the immunohistochemical secondary antibody diluent, and after adding the secondary antibody, it was protected from light for 2h at room temperature.
The secondary antibody was discarded and washed 3 times with PBS for 5 min each time. An appropriate amount of PBS was added, and the mixture was observed under a Leica fluorescence microscope and photographed.
And observing the regeneration condition of the protrusions, photographing and counting the distribution of the lengths of the protrusions of each group.
The results are shown in fig. 2, in which fig. 2A is a comparative graph of the transfection of the mic Negative control (mic-NC, Negative control) or miR-25-3P mimics, respectively, into DRG neurons cultured in vitro, and fig. 2B is the average length of the DRG neuron axon growth under Bar =100 μm or Bar =250 μm, < 0.01. As can be seen, the overexpression of miR-25-3p (miR-25-3 p mimics) can obviously promote the growth of DRG neuron axons.
S3: in vitro overexpression of miR-25-3p for inhibiting expression of Pten in cortical neurons
C1: culturing primary cortical neuronal cells
Cortical neurons were obtained from SD rats by 18 days of pregnancy, taking out cerebral cortex, placing into dissecting fluid HA, adding appropriate amount of 0.25% pancreatin, digesting at 37 deg.C for 20 min. Pancreatin was stopped with DMEM containing 10% fetal bovine serum, and the supernatant was discarded after centrifugation. The cells were resuspended in DMEM containing 10% FBS, passed through a 70 μm mesh screen, and the supernatant discarded by centrifugation. 10% FBS DMEM heavy suspension cells, after counting, with 2 x 107Cell number per well into 6-well plates coated with polylysine
C2: neuronal cell mimics transfection
After the cells are cultured for 4 hours and adhere to the wall, the cells are added into the cultured neurons after being mixed with Lipofectamine RNAiMAX Reagent uniformly, negative control (20 nM final concentration, Yangzhou Sharp biology company) and Neurobasal culture medium of 2% B-27 and 2mM glutamine, and the cultured neurons are replaced by the neuron culture medium without transfection Reagent after being cultured for 12 hours.
C3：Western blot
Collecting the cortical neuron cells cultured for 3d in vitro, rinsing with PBS, adding appropriate amount of cell lysate (containing 1% protease inhibitor), and performing ice lysis for 5-10 min until the cells are completely lysed; centrifugation was carried out at 13000 rpm for 10min at 4 ℃ to collect the supernatant. And (4) quantifying the protein by using the BCA method. SDS-PAGE was performed, and after membrane transfer, the cells were blocked with 5% skim milk at room temperature for 2 hours. Primary antibody was incubated, and PTEN (1: 1000, cell signalling) was diluted with primary antibody diluent and incubated at room temperature overnight. Wash 3 times with 1 × TBS for 10min each time. The secondary goat anti-rabbit HRP (1: 2500, abcam) was diluted with 5% skim milk and incubated at room temperature for 120 min. 1 × TBST 3 times, 10min each, 1 × TBS 1 times, 10 min. And incubating ECL developing solution on the membrane for 1-3 min at room temperature. And developing and observing the result. And (5) after the film is dried, transmitting the result to a computer by using a film scanner. The Western blot result is shown in FIG. 3, wherein FIG. 3A is a graph showing that Mimic Negative control (Mimic-NC, Negative control) or miR-25-3p mimics transfects DRG neurons cultured in vitro respectively, FIG. 2B is a PTEN protein expression condition detected by Western blot after 72 h, and the internal reference is beta-actin. B,. P < 0.0001. The result shows that compared with the Mimic Negative control group, the protein level of PTEN in cortical neurons can be remarkably inhibited by over-expressing miR-25-3 p.
The above description is only an example of the present invention, and is not intended to limit the present invention, and it is obvious to those skilled in the art that various modifications and variations can be made in the present invention. Any modification, equivalent replacement, or improvement made within the spirit and principle of the present invention should be included in the scope of the claims of the present invention.

Claims (7)

1. A miR-25-3p, which is characterized in that: as a molecular intervention target, miR-25-3p is overexpressed and is used for promoting the growth of axons of DGR neurons and cortical neurons.
2. The application of miR-25-3p is characterized in that: the miR-25-3p participates in the repair of peripheral nerve injury by regulating the axonal growth of DGR neurons.
3. The use of miR-25-3p according to claim 2, wherein: the miR-25-3p participates in central nerve injury repair by regulating the growth of cortical neuron axons.
4. An application method of miR-25-3p is characterized by comprising the following steps:
s1: the miR-25-3p is expressed in vitro to promote the growth of the axon of cortical neurons;
s2: in vitro miR-25-3p expression promotes DRG neuron axon growth;
s3: overexpression of miR-25-3p in vitro inhibits Pten expression in cortical neurons.
5. The method for the use of miR-25-3p according to claim 4, wherein: the specific steps in the step S1 are as follows:
a1: culturing primary cortical neuronal cells;
a2: transfecting neuron cells with mimics;
a3: cellular immunofluorescent stain axon growth length measurement.
6. The method for the use of miR-25-3p according to claim 4, wherein: the specific steps in the step S2 are as follows:
b1: culturing primary DRG neuron cells;
b2: transfecting neuron cells with mimics;
b3: cellular immunofluorescence staining and axon regeneration length measurement.
7. The method for using miR-25-3p according to claim 4, characterized in that: the specific steps in the step S3 are as follows:
c1: culturing primary cortical neuronal cells;
c2: transfecting neuron cells with mimics;
C3：Western blot。
CN202111329966.6A 2021-11-11 2021-11-11 miR-25-3p, application and application method thereof Pending CN114085833A (en)

Priority Applications (1)

Application Number Priority Date Filing Date Title
CN202111329966.6A CN114085833A (en) 2021-11-11 2021-11-11 miR-25-3p, application and application method thereof

Applications Claiming Priority (1)

Application Number Priority Date Filing Date Title
CN202111329966.6A CN114085833A (en) 2021-11-11 2021-11-11 miR-25-3p, application and application method thereof

Publications (1)

Publication Number Publication Date
CN114085833A true CN114085833A (en) 2022-02-25

Family

ID=80299746

Family Applications (1)

Application Number Title Priority Date Filing Date
CN202111329966.6A Pending CN114085833A (en) 2021-11-11 2021-11-11 miR-25-3p, application and application method thereof

Country Status (1)

Country Link
CN (1) CN114085833A (en)

Citations (1)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
CN112301033A (en) * 2020-11-24 2021-02-02 南通大学 miR-30a-5p and application thereof in promoting nerve regeneration and repairing peripheral nerve injury

Patent Citations (1)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
CN112301033A (en) * 2020-11-24 2021-02-02 南通大学 miR-30a-5p and application thereof in promoting nerve regeneration and repairing peripheral nerve injury

Non-Patent Citations (2)

* Cited by examiner, † Cited by third party
Title
YANZHUO ZHANG ET AL.: "Inhibition of miR-25 aggravates diabetic peripheral neuropathy", CELLULAR, MOLECULAR AND DEVELOPMENTAL NEUROSCIENCE *
刘勇等: "坐骨神经预处理后mir-25-3p促进大鼠脊髓后索损伤修复", 中国优秀硕士学位论文全文数据库医药卫生科技辑 *

Similar Documents

Publication Publication Date Title
JP6698753B2 (en) 3D heterogeneous tissue culture
AU2022200207B2 (en) Compositions and methods for induced tissue regeneration in mammalian species
US9725737B2 (en) Chondrocyte-like cell, and method for producing same
US20210095260A1 (en) Bi- or multi-differentiated organoid
JP5759536B2 (en) Corneal epithelial differentiation-directed iPS cells
Barretto et al. ASCL1-and DLX2-induced GABAergic neurons from hiPSC-derived NPCs
CN112301033B (en) miR-30a-5p and application thereof in promoting nerve regeneration and repairing peripheral nerve injury
Tanaka et al. Human induced pluripotent stem cell-derived salivary gland organoids model SARS-CoV-2 infection and replication
CN104781396A (en) Activation of innate immunity for nuclear reprogramming of somatic cells
CN114085833A (en) miR-25-3p, application and application method thereof
JP2019506899A (en) Method for producing renal cells from differentiated cells
Eintracht et al. Efficient embryoid-based method to improve generation of optic vesicles from human induced pluripotent stem cells
CN115851940A (en) Osteosarcoma molecular marker and application thereof
JP2010246476A (en) Cardiomyocyte differentiation inducing promoter and use thereof
CN103571793A (en) Method of regulating and controlling retinal progenitor cell generated by inducing
CN111643681A (en) Application of Nr4a3 in promoting nerve regeneration and repairing nerve injury
Carido et al. Reliability of human retina organoid generation from hiPSC-derived neuroepithelial cysts
US20240093144A1 (en) Differential adhesion and tension guided formation of stem cell derived embryos
Wijesinghe et al. Adult porcine (Sus scrofa) derived inner ear cells possessing multipotent stem/progenitor cell characteristics in in vitro cultures
Parreno et al. TPM3. 1 association with actin stress fibers is required for lens epithelial to mesenchymal transition
Kuwar et al. Generation of induced pluripotent stem cells from rat fibroblasts and optimization of its differentiation into mature functional neurons
Knaus et al. Reorganization of Septin structures regulates early myogenesis
Mayerl et al. Optimizing AAV-based gene delivery to photoreceptors in hPSC-derived retinal organoids
CN116688133A (en) Application of Tgif1 as molecular target in preparation of drugs for promoting nerve regeneration and repairing nerve injury
CN117070608A (en) Method for detecting later-B as treatment target for remyelination of peripheral nerve

Legal Events

Date Code Title Description
PB01 Publication
PB01 Publication
SE01 Entry into force of request for substantive examination
SE01 Entry into force of request for substantive examination