Open AccessBMSC s and miR‐124a ameliorated diabetic nephropathy via inhibiting notch signalling pathway
Author(s) -
Sun Jiping,
Zhao Fei,
Zhang Wenjing,
Lv Jia,
Lv Jing,
Yin Aiping
Publication year - 2018
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.13747
Subject(s) - notch signaling pathway , diabetic nephropathy , apoptosis , chemistry , mesenchymal stem cell , flow cytometry , microbiology and biotechnology , tunel assay , progenitor cell , islet , biology , stem cell , signal transduction , kidney , endocrinology , insulin , biochemistry
BMSC s are important in replacement therapy of diabetic nephropathy ( DN ). MiR‐124a exerts effect on the differentiation capability of pancreatic progenitor cells. The objective of this study was to explore the molecular mechanisms, the functions of miR‐124a and bone marrow mesenchymal stem cells ( BMSC s) in the treatment of DN . Characterizations of BMSC s were identified using the inverted microscope and flow cytometer. The differentiations of BMSC s were analysed by immunofluorescence assay and DTZ staining. The expression levels of islet cell‐specific transcription factors, apoptosis‐related genes, podocytes‐related genes and Notch signalling components were detected using quantitative real‐time reverse transcription PCR ( qRT ‐ PCR ) and Western blot assays. The production of insulin secretion was detected by adopting radioimmunoassay. Cell proliferation and apoptosis abilities were detected by CCK ‐8, flow cytometry and TUNEL assays. We found that BMSC s was induced into islet‐like cells and that miR‐124a could promote the BMSC s to differentiate into islet‐like cells. BMSC s in combination with miR‐124a regulated islet cell‐specific transcription factors, apoptosis‐related genes, podocytes‐related genes as well as the activity of Notch signalling pathway. However, BMSC s in combination with miR‐124a relieved renal lesion caused by DN and decreased podocyte apoptosis caused by HG . The protective effect of BMSC s in combination with miR‐124a was closely related to the inactivation of Notch signalling pathway. MSC s in combination with miR‐124a protected kidney tissue from impairment and inhibited nephrocyte apoptosis in DN .