Combined action of hypoxia and hypercapnia on functional state of the respiratory center

Kulik, Ákos; Kondrat'eva, L. N.

doi:10.1007/bf00832704

Cited by 4 publications

(1 citation statement)

References 3 publications

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“…MSCs were procured from Shanghai Zhong Qiao Xin Zhou Biotechnology (Shanghai, China), which were tested for purity by flow cytometry and for their ability to differentiate into osteogenic, chondrogenic, and adipogenic lineages. [18] MSC purity was validated and positive for CD44 [19] and negative for CD45, CD11b, CD90, and CD117 [20,21] by Flow Cytometry analysis. All experiments used cells between passages 4-10.…”

Section: Preparation Of Conditioned Medium (Cm)mentioning

confidence: 99%

Lipopolysaccharides protect mesenchymal stem cell against cardiac ischemia-reperfusion injury by HMGB1/STAT3 signaling

WEN,

PENG,

WANG

et al. 2023

Journal of Geriatric Cardiology

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BACKGROUND Myocardial ischemia-reperfusion (I/R) is a serious and irreversible injury. Bone marrow-derived mesenchymal stem cells (MSCs) is considered to be a potential therapy for I/R injury due to the paracrine effects. High-mobility group box 1 (HMGB1) is a novel mediator in MSC and regulates the response of inflammation injury. Signal Transduction and Transcription Activator 3 (STAT3) is a critical transcription factor and important for release of paracrine factors. However, the relationship between HMGB1 and STAT3 in paracrine effect of MSC remains unknown. METHODSIn vitro, hypoxia/reoxygenation injury model was established by AnaeroPack System and examined by Annexin V flow cytometry, CCK8 assay and morphology observation. Detection of apoptotic proteins and protein expression of HMGB1 and STAT3 by Western blot. RESULTSThe conditioned medium of MSCs with or without LPS pretreatment was cocultured with H9C2 cells for 24 h before hypoxia treatment and MSC showed obvious cardiomyocytes protect role, as evidence by decreased apoptosis rate and improved cells viability, and LPS pretreated MSC exhibited better protect role than untreated MSC. However, such effect was abolished in HMGB1 deficiency group, silencing HMGB1 decreased the secretion of vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), insulin growth factor (IGF), cell viability, and the expression of STAT3. Furthermore, STAT3 silence attenuated the protective effect of LPS in MSC.CONCLUSIONS These findings suggested that LPS improved MSC-mediated cardiomyocytes protection by HMGB1/STAT3 signaling.

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Section: Preparation Of Conditioned Medium (Cm)mentioning

confidence: 99%