PMID- 31119778
OWN - NLM
STAT- MEDLINE
DCOM- 20200909
LR  - 20211204
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 120
IP  - 10
DP  - 2019 Oct
TI  - Bradykinin protects cardiac c-kit positive cells from high-glucose-induced 
      senescence through B2 receptor signaling pathway.
PG  - 17731-17743
LID - 10.1002/jcb.29039 [doi]
AB  - Cardiac c-kit positive cells are cardiac-derived cells that exist within the 
      heart and have a great many protective effects. The senescence of cardiac c-kit 
      positive cells probably leads to cell dysfunction. Bradykinin plays a key role in 
      cell protection. However, whether bradykinin prevents cardiac c-kit positive 
      cells from high-glucose-induced senescence is unknown. Here, we found that 
      glucose treatment causes the premature senescence of cardiac c-kit positive 
      cells. Bradykinin B2 receptor (B2R) expression was declined by glucose-induced 
      senescence. Bradykinin treatment inhibited senescence and reduced intracellular 
      oxygen radicals according to senescence-associated beta-galactosidase staining and 
      2',7'-dichlorodihydrofluorescein diacetate staining. Moreover, the mitochondrial 
      membrane potential was damaged, as measured by JC-1 staining. The mitochondrial 
      membrane potential was preserved under bradykinin treatment. The concentration of 
      superoxide was decreased, and the concentration of intracellular adenosine 
      triphosphate was increased after bradykinin treatment. Western blot showed that 
      bradykinin leads to AKT and mammalian target of rapamycin (mTOR) phosphorylation 
      and decreased levels of P53 and P16 when compared with glucose treatment alone. 
      Antagonists of B2R, phosphoinositide 3-kinase (PI3K), mTOR, and B2R small 
      interfering RNA prevented the protective effect of bradykinin. P53 antagonist 
      also inhibited the glucose-induced senescence of cardiac c-kit positive cells. In 
      conclusion, bradykinin prevents the glucose-induced premature senescence of 
      cardiac c-kit positive cells through the B2R/PI3K/AKT/mTOR/P53 signal pathways.
CI  - (c) 2019 Wiley Periodicals, Inc.
FAU - Fu, Cong
AU  - Fu C
AD  - Department of Cardiology, Yi Ji Shan hospital affiliated to Wan Nan Medical 
      College, Wuhu, AnHui, China.
AD  - Department of Cardiology, Zhong Da hospital affiliated to Southeast University, 
      Nanjing, JiangSu, China.
AD  - Key Laboratory of Non-coding RNA Transformation Research of Anhui Higher 
      Education Institution, Wann Nan Medical College, Wuhu, AnHui, China.
FAU - Cao, Yuhan
AU  - Cao Y
AD  - Key Laboratory of Non-coding RNA Transformation Research of Anhui Higher 
      Education Institution, Wann Nan Medical College, Wuhu, AnHui, China.
AD  - Department of Nephrology, Yi Ji Shan Hospital affiliated to Wan Nan Medical 
      College, Wuhu, Anhui, China.
FAU - Li, Bing
AU  - Li B
AD  - Department of Cardiology, Zhong Da hospital affiliated to Southeast University, 
      Nanjing, JiangSu, China.
FAU - Xu, Rongfeng
AU  - Xu R
AD  - Department of Cardiology, Zhong Da hospital affiliated to Southeast University, 
      Nanjing, JiangSu, China.
FAU - Sun, Yuning
AU  - Sun Y
AD  - Department of Cardiology, Zhong Da hospital affiliated to Southeast University, 
      Nanjing, JiangSu, China.
FAU - Yao, Yuyu
AU  - Yao Y
AUID- ORCID: 0000-0001-7841-288X
AD  - Department of Cardiology, Zhong Da hospital affiliated to Southeast University, 
      Nanjing, JiangSu, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190522
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Cardiotonic Agents)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptor, Bradykinin B2)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - IY9XDZ35W2 (Glucose)
RN  - S8TIM42R2W (Bradykinin)
SB  - IM
MH  - Adenosine Triphosphate/metabolism
MH  - Animals
MH  - Bradykinin/*pharmacology
MH  - Cardiotonic Agents/*pharmacology
MH  - Cells, Cultured
MH  - Cellular Senescence/drug effects
MH  - Glucose/*toxicity
MH  - Male
MH  - Membrane Potential, Mitochondrial/drug effects
MH  - Mice, Inbred C57BL
MH  - Myocardium/*metabolism/*pathology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Proto-Oncogene Proteins c-kit/*metabolism
MH  - RNA, Small Interfering/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Receptor, Bradykinin B2/*metabolism
MH  - *Signal Transduction/drug effects
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Tumor Suppressor Protein p53/metabolism
OTO - NOTNLM
OT  - B2 receptor
OT  - bradykinin
OT  - cardiac c-kit positive cells
OT  - senescence
EDAT- 2019/05/24 06:00
MHDA- 2020/09/10 06:00
CRDT- 2019/05/24 06:00
PHST- 2018/12/21 00:00 [received]
PHST- 2019/05/01 00:00 [revised]
PHST- 2019/05/03 00:00 [accepted]
PHST- 2019/05/24 06:00 [pubmed]
PHST- 2020/09/10 06:00 [medline]
PHST- 2019/05/24 06:00 [entrez]
AID - 10.1002/jcb.29039 [doi]
PST - ppublish
SO  - J Cell Biochem. 2019 Oct;120(10):17731-17743. doi: 10.1002/jcb.29039. Epub 2019 
      May 22.