Effects of porcine STC-1 on cell metabolism and mitochondrial function

Yang, Kaidian; Yang, Yuefei; Qi, Chuanxiang; Ju, Huiming

doi:10.1016/j.ygcen.2019.113298

Cited by 10 publications

(7 citation statements)

References 21 publications

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“…To elucidate the potential reendothelialization effect of S-ADSC-Exo on post-injury carotid endarterium, possibilities for the related proteins were explored. STC-1 is indicated to be an endogenous regulator of ROS [35], and ROS is the key signal to activate NLRP3 in ammasome [36]. ROS is a major mediator of the in ammation follows mechanical injury of endovascular treatment.…”

Section: Discussionmentioning

confidence: 99%

Exosomes from Adipose Mesenchymal Stem Cells Overexpressing Stanniocalcin-1 Promote Reendothelialization After Carotid Endarterium Mechanical Injury

Liu

Shi

Peng

et al. 2021

Stem Cell Rev and Rep

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Stanniocalcin-1 (STC-1) is a secreted glycoprotein that participates in the regulation of in ammation, apoptosis, and necrosis. We investigated the reendothelialization effect of exosomes from adipose stem cells (ADSC) overexpressing STC-1 on injured carotid endarterium. ADSCs were transfected with lentivirus vectors containing pre-STC-1. PHK-26 as molecular probe was used to track the exosomes engulfed by mice arterial endothelial cells (MAEC). The role of STC-1-ADSC-Exosome (S-ADSC-Exo) in MAECs was veri ed through scratch test and tube forming. Expressions of STC-1 and NLRP3 in ammasome were detected by western blot and quantitative reverse transcription polymerase chain reaction. Reendothelialization effect was inhibited by the antagonist of siRNA targeting STC-1. Carotid endarterium mechanical injury was induced by insertion with a guidewire into the common carotid artery lumen. Carotid arteries were harvested for histological examination, immuno uorescence staining, and Evan's blue staining. Transfection of STC-1 signi cantly enhanced STC-1 levels in ADSCs, their exosomes, and MAECs. Compared with the control group and the ADSC-Exo group, STC-1 enriched exosomes markedly inhibited the expressions of NLRP3, Caspase-1, and IL-1β in MAECs, exhibited good lateral migration capacity, and promoted angiogenesis. Administration of siRNA targeting STC-1 completely abolished down-regulation of NLRP3, Caspase-1, and IL-1β by STC-1 and inhibited effects of S-ADSC-Exo on lateral migration and angiogenesis. In vivo administration of S-ADSC-Exo had reendothelialization effect on post-injury carotid endarterium as evidenced by thinner arterial wall, low-expressed NLRP3 in ammasome, and more living endothelial cells. The reendothelialization effect of exosomes from ADSCs on post-injury carotid endarterium can be enhanced by genetic modi cation to contain elevated STC-1.

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Section: Discussionmentioning

confidence: 99%

Exosomes from Adipose Mesenchymal Stem Cells Overexpressing Stanniocalcin-1 Promote Reendothelialization After Carotid Endarterium Mechanical Injury

Liu

Shi

Peng

et al. 2021

Stem Cell Rev and Rep

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show abstract

“…STC1, as well as STC2, was originally identified as a calcium/phosphate-regulating hormone. Recent studies have indicated that the STC-1 gene is closely related to glucose and lipid metabolism as well as to mitochondrial function [ 29 , 30 ]. In addition, PARP or PAR alterations have been described in tumors, specifically those influencing EMT [ 31 – 33 ].…”

Section: Discussionmentioning

confidence: 99%

LAIR-1 overexpression inhibits epithelial–mesenchymal transition in osteosarcoma via GLUT1-related energy metabolism

et al. 2020

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Background: Leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1) is a collagen receptor belonging to the immunoglobulin superfamily. Although previous studies have evaluated the biological role of LAIR in solid tumors, the precise mechanisms underlying the functions of LAIR-1 as a regulator of tumor biological functions remain unclear. Methods: LAIR-1 expression was evaluated by immunohistochemical analysis using an osteosarcoma (OS) tissue microarray. Wound healing and transwell migration assays were performed to evaluate tumor cell migration. Quantitative real-time polymerase chain reaction (qPCR) and western blotting were conducted to detect the expression of epithelial-mesenchymal transition (EMT)-related molecules. RNA-sequencing (RNA-seq) was conducted to evaluate the mRNA expression profiles after overexpressing LAIR-1 in OS cells. Glucose transporter (Glut)1 expression in OS cells was evaluated by western blotting. Results: LAIR-1 expression was significantly different between the T1 and T2 stages of OS tumors, and it inhibited OS cell migration. LAIR-1 expression was inversely correlated with the expression of Twist1, an EMT-associated transcription factor, via the Forkhead box O1 signal transduction pathway. Furthermore, RNA-seq and qPCR demonstrated that the expression of EMT energy metabolism-related molecules was significantly reduced after LAIR-1 overexpression. Conclusions: LAIR-1 overexpression decreased the expression of Glut1 and inhibited the expression of EMT-related molecules in OS cells. These findings provide new insights into the molecular mechanism underlying OS progression.

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“…STC1, as well as STC2, was originally identi ed as a calcium/phosphate-regulating hormone. Recent studies have indicated that the STC-1 gene is closely related to glucose and lipid metabolism as well as to mitochondrial function [29,30]. In addition, PARP or PAR alterations have been described in tumors, speci cally those in uencing EMT [31][32][33].…”

Section: Discussionmentioning

confidence: 99%

LAIR-1 overexpression inhibits epithelial–mesenchymal transition in osteosarcoma via GLUT1-related energy metabolism

Zhang

Cheng

et al. 2020

Preprint

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Background: Leukocyte-associated immunoglobulin-like receptor-1 (LAIR-1) is a collagen receptor belonging to the immunoglobulin superfamily. Although previous studies have evaluated the biological role of LAIR in solid tumors, the precise mechanisms underlying the functions of LAIR-1 as a regulator of tumor biological functions remain unclear.Methods: LAIR-1 expression was evaluated by immunohistochemical analysis using an osteosarcoma (OS) tissue microarray. Wound healing and transwell migration assays were performed to evaluate tumor cell migration. Quantitative real-time polymerase chain reaction (qPCR) and western blotting were conducted to detect the expression of epithelial–mesenchymal transition (EMT)-related molecules. RNA-sequencing (RNA-seq) was conducted to evaluate the mRNA expression profiles after overexpressing LAIR-1 in OS cells. Glucose transporter (Glut)1 expression in OS cells was evaluated by western blotting.Results: LAIR-1 expression was significantly different between the T1 and T2 stages of OS tumors, and it inhibited OS cell migration. LAIR-1 expression was inversely correlated with the expression of Twist1, an EMT-associated transcription factor, via the Forkhead box O1 signal transduction pathway. Furthermore, RNA-seq and qPCR demonstrated that the expression of EMT energy metabolism-related molecules was significantly reduced after LAIR-1 overexpression.Conclusions: LAIR-1 overexpression decreased the expression of Glut1 and inhibited the expression of EMT-related molecules in OS cells. These findings provide new insights into the molecular mechanism underlying OS progression.

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Effects of porcine STC-1 on cell metabolism and mitochondrial function

Cited by 10 publications

References 21 publications

Exosomes from Adipose Mesenchymal Stem Cells Overexpressing Stanniocalcin-1 Promote Reendothelialization After Carotid Endarterium Mechanical Injury

Exosomes from Adipose Mesenchymal Stem Cells Overexpressing Stanniocalcin-1 Promote Reendothelialization After Carotid Endarterium Mechanical Injury

LAIR-1 overexpression inhibits epithelial–mesenchymal transition in osteosarcoma via GLUT1-related energy metabolism

LAIR-1 overexpression inhibits epithelial–mesenchymal transition in osteosarcoma via GLUT1-related energy metabolism

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