Increased Prolylcarboxypeptidase Expression Can Serve as Biomarker of Senescence in Culture DOI Open Access

Nicholas Boullard,

Jason J. Paris,

Zia Shariat‐Madar

et al.

Published: March 28, 2024

Prolylcarboxypeptidase (PRCP, PCP, Lysosomal Pro-X-carboxypeptidase, Angiotensinase C) controls angiotensin - and kinin- induced cell signaling. Elevation of PRCP appear to be activated in chronic inflammatory diseases (cardiovascular disease (CVD), diabetes) proportion severity. Vascular endothelial senescence mitochondrial dysfunction have consistently been shown models CVD aging. The cellular senescence, a driver age-related dysfunction, can differentially alter the expression lysosomal enzymes due membrane permeability. There is lack data demostrating effect on function PRCP. To explore changes PRCP, PRCP-dependent prekallikrein (PK) pathway was charcterized early – late-passage human pulmonary artery cells (HPAECs). Detailed kinetic analysis treated with high molecular weight kininogen (HK), precursor bradykinin (BK), PK revealed mechansim by which senescent HPAECs activate generation kallikrein upon assembly HK-PK complex parallel an upregulation nitric oxide (NO) synthase (eNOS) NO formation. production both eNOS increased early-passage while decreased HPAECs. Low activity late passage associated rapid telomerase reverse transcriptase mRNA levels. We also found that, increase number HPAECs, reduced altered respiration rate. These results indicated that aging dysregulates protein expression, further studies will shed light into complexity signling

Language: Английский

Increased Prolylcarboxypeptidase Expression Can Serve as Biomarker of Senescence in Culture DOI Open Access

Nicholas Boullard,

Jason J. Paris,

Zia Shariat‐Madar

et al.

Published: March 28, 2024

Prolylcarboxypeptidase (PRCP, PCP, Lysosomal Pro-X-carboxypeptidase, Angiotensinase C) controls angiotensin - and kinin- induced cell signaling. Elevation of PRCP appear to be activated in chronic inflammatory diseases (cardiovascular disease (CVD), diabetes) proportion severity. Vascular endothelial senescence mitochondrial dysfunction have consistently been shown models CVD aging. The cellular senescence, a driver age-related dysfunction, can differentially alter the expression lysosomal enzymes due membrane permeability. There is lack data demostrating effect on function PRCP. To explore changes PRCP, PRCP-dependent prekallikrein (PK) pathway was charcterized early – late-passage human pulmonary artery cells (HPAECs). Detailed kinetic analysis treated with high molecular weight kininogen (HK), precursor bradykinin (BK), PK revealed mechansim by which senescent HPAECs activate generation kallikrein upon assembly HK-PK complex parallel an upregulation nitric oxide (NO) synthase (eNOS) NO formation. production both eNOS increased early-passage while decreased HPAECs. Low activity late passage associated rapid telomerase reverse transcriptase mRNA levels. We also found that, increase number HPAECs, reduced altered respiration rate. These results indicated that aging dysregulates protein expression, further studies will shed light into complexity signling

Language: Английский

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