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http://purl.uniprot.org/citations/32432759http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32432759http://www.w3.org/2000/01/rdf-schema#comment"

Objective

To clarify the role of HOXA-AS2 in the progression of diabetic nephropathy (DN) and the molecular mechanism.

Materials and methods

Relative levels of HOXA-AS2 and microRNA-302b-3p (miRNA-302b-3p) in serum and kidney tissues of DN rats induced by STZ administration and controls were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Serum levels of interleukin-1β (IL-1β), Transforming Growth Factor-α (TNF-α), creatinine, and BUN, as well as blood glucose in DN rats administrated with vector or pcDNA-HOXA-AS2 lentivirus, were detected. Dual-Luciferase reporter gene assay was conducted to verify the interaction among HOXA-AS2, miRNA-302b-3p, and TIMP3. At last, the regulatory effects of HOXA-AS2/miRNA-302b-3p/TIMP3 axis on levels of IL-1β and TNF-α, proliferative, and apoptotic rates in podocytes undergoing high-level glucose treatment were explored.

Results

HOXA-AS2 was downregulated in STZ-induced DN rats. In vivo overexpression of HOXA-AS2 alleviated kidney injuries in DN rats, manifesting as elevations on serum levels of IL-1β, TNF-α, creatinine, BUN, and blood glucose. HOXA-AS2/miRNA-302b-3p/TIMP3 axis protected DN-induced inflammatory response, proliferation suppression, and apoptosis in podocytes following the high-glucose treatment.

Conclusions

HOXA-AS2/miRNA-302b-3p/TIMP3 axis protects inflammatory response, proliferation suppression, and apoptosis in podocytes treated with high-level glucose, thus alleviating the deterioration of DN."xsd:string
http://purl.uniprot.org/citations/32432759http://purl.org/dc/terms/identifier"doi:10.26355/eurrev_202005_21187"xsd:string
http://purl.uniprot.org/citations/32432759http://purl.uniprot.org/core/author"Li X."xsd:string
http://purl.uniprot.org/citations/32432759http://purl.uniprot.org/core/author"Yu H.M."xsd:string
http://purl.uniprot.org/citations/32432759http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32432759http://purl.uniprot.org/core/name"Eur Rev Med Pharmacol Sci"xsd:string
http://purl.uniprot.org/citations/32432759http://purl.uniprot.org/core/pages"4963-4970"xsd:string
http://purl.uniprot.org/citations/32432759http://purl.uniprot.org/core/title"Overexpression of HOXA-AS2 inhibits inflammation and apoptosis in podocytes via sponging miRNA-302b-3p to upregulate TIMP3."xsd:string
http://purl.uniprot.org/citations/32432759http://purl.uniprot.org/core/volume"24"xsd:string
http://purl.uniprot.org/citations/32432759http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/32432759
http://purl.uniprot.org/citations/32432759http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/32432759
http://purl.uniprot.org/uniprot/#_F7FFD0-mappedCitation-32432759http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32432759
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http://purl.uniprot.org/uniprot/#_P48032-mappedCitation-32432759http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32432759
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http://purl.uniprot.org/uniprot/P48032http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/32432759