PMID- 35290144
OWN - NLM
STAT- MEDLINE
DCOM- 20220411
LR  - 20220716
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 3
DP  - 2022 Mar
TI  - Downregulation of secreted frizzled-related protein 4 inhibits 
      hypoxia/reoxygenation injury in diabetic cardiomyocytes by protein tyrosine 
      phosphatase nonreceptor type 12.
PG  - 7697-7708
LID - 10.1080/21655979.2022.2034706 [doi]
AB  - Myocardial ischemia-reperfusion injury in diabetic patients leads to an increased 
      incidence of complications and mortality. Secreted frizzled-related protein 4 
      (SFRP4) plays a critical role in diabetic myocardial ischemia-reperfusion. This 
      paper aims to uncover the underlying mechanisms of SFRP4 in hypoxia/reoxygenation 
      (H/R) injury of diabetic myocardial cells. An in vitro ischemia/reperfusion (I/R) 
      injury model was established using high glucose-induced H9c2 cardiomyocytes. 
      Expression of SFRP4 was detected by real-time reverse transcriptase-polymerase 
      chain reaction and Western blotting. After transfection of SFRP4, the binding of 
      SFRP4 to protein tyrosine phosphatase nonreceptor type 12 (PTPN12) was predicted 
      by database and verified by co-immunoprecipitation assay. P13 K/AKT protein 
      levels were examined by Western blotting. PTPN12 levels were tested by RT-qPCR 
      and Western blotting, cell viability by Cell Counting Kit-8, lactose 
      dehydrogenase kit, terminal dUTP nick-end labeling assay, and cell inflammation 
      and oxidative stress by Western blotting and enzyme linked immunosorbent assay. 
      After overexpression of PTPN12, the experiments for cell viability, inflammation 
      and oxidative stress were repeated once more. SFRP4 expression was upregulated in 
      a high-glucose-stimulated H/R cardiomyocyte model. The interference of SFRP4 
      promoted cell viability, inhibited the inflammatory and oxidative stress response 
      of H/R cardiomyocytes induced by high glucose. SFRP4 interacted with PTPN12 and 
      inhibited the PI3K/AKT signaling pathway. PTPN12 overexpression reversed the 
      inhibitory effect of sh-SFRP4 on H/R cardiomyocyte damage induced by high 
      glucose. Downregulation of SFRP4 inhibited H/R cell damage in diabetic 
      cardiomyocytes by binding to PTPN12.
FAU - Bai, Zhifeng
AU  - Bai Z
AD  - Second Department of Cardiovascular Medicine, The First People's Hospital of 
      Shangqiu City, Shangqiu, China.
FAU - Hao, Xiuhong
AU  - Hao X
AD  - Second Department of Cardiovascular Medicine, The First People's Hospital of 
      Shangqiu City, Shangqiu, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (WD repeat containing planar cell polarity effector)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 3.1.3.48 (PTPN12 protein, human)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 12)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatases)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Apoptosis/genetics
MH  - *Diabetes Mellitus
MH  - Down-Regulation
MH  - Glucose/metabolism/toxicity
MH  - Humans
MH  - Hypoxia/metabolism
MH  - Inflammation/metabolism
MH  - Intracellular Signaling Peptides and Proteins
MH  - *Myocytes, Cardiac/metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Protein Tyrosine Phosphatase, Non-Receptor Type 12/metabolism
MH  - Protein Tyrosine Phosphatases/metabolism/pharmacology
MH  - Proto-Oncogene Proteins c-akt/metabolism
PMC - PMC9278962
OTO - NOTNLM
OT  - H/R injury
OT  - PI3K/AKT
OT  - PTPN12
OT  - SFRP4
OT  - diabetic cardiomyocytes
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/03/16 06:00
MHDA- 2022/04/12 06:00
PMCR- 2022/03/15
CRDT- 2022/03/15 17:17
PHST- 2022/03/15 17:17 [entrez]
PHST- 2022/03/16 06:00 [pubmed]
PHST- 2022/04/12 06:00 [medline]
PHST- 2022/03/15 00:00 [pmc-release]
AID - 2034706 [pii]
AID - 10.1080/21655979.2022.2034706 [doi]
PST - ppublish
SO  - Bioengineered. 2022 Mar;13(3):7697-7708. doi: 10.1080/21655979.2022.2034706.