Oxidized low‐density lipoprotein (ox‐<scp>LDL</scp>) promotes cardiac differentiation of bone marrow mesenchymal stem cells via activating <scp>ERK</scp>1/2 signaling

Zhang, Fenxi; Wang, Congrui; Lin, Juntang; Wang, Xianwei

doi:10.1111/1755-5922.12305

Cited by 5 publications

(3 citation statements)

References 24 publications

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“…a previous study reported that the MaPK signaling pathway, including erK1/2, JnK and p38 MaPK molecules, is activated in chondrocytes (19). activation of erK signaling pathway can enhance the ability of MScs to differentiate into osteoblasts and cardiomyocytes (20,21). in addition, the erK1/2 signaling pathway regulates chondrocyte differentiation and cartilage formation in in vitro (22).…”

Section: Effect Of Cd44 On Differentiation Of Human Amniotic Mesenchymentioning

confidence: 95%

Effect of CD44 on differentiation of human amniotic mesenchymal stem cells into chondrocytes via Smad and ERK signaling pathways

Wang

et al. 2020

Mol Med Report

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cd44 antigen (cd44) is a transmembrane protein found in cell adhesion molecules and is involved in the regulation of various physiological processes in cells. it was hypothesized that cd44 directly affected the chondrogenic differentiation of human amniotic mesenchymal stem cells (haMScs). in the present study, the expression of chondrocyte-associated factors was detected in the absence and presence of the antibody blocker anti-cd44 antibody during the chondrogenic differentiation of haMScs. Following inhibition of cd44 expression, the transcriptional levels of chondrocyte-associated genes SrY-box transcription factor 9, aggrecan and collagen type ii α 1 chain, as well as the production of chondrocyte markers type ii collagen and aggrecan were significantly decreased in haMScs. Further investigation indicated that there was no significant change in total erK1/2 expression following inhibition of cd44 expression; however, phosphorylated (p)-erK1/2 expression was decreased. The expression of p-Smad2/3 was also upregulated following cd44 inhibition. These data indicated that cd44 may affect the differentiation of haMScs into chondrocytes by regulating the Smad2/3 and erK1/2 signaling pathway.

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Section: Effect Of Cd44 On Differentiation Of Human Amniotic Mesenchymentioning

confidence: 95%

Effect of CD44 on differentiation of human amniotic mesenchymal stem cells into chondrocytes via Smad and ERK signaling pathways

Wang

et al. 2020

Mol Med Report

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“…In mouse MSCs, properties important for engraftment (e.g., proliferation, migration, and adhesion) were stimulated by oxLDLs through activation of LOX-1 and expression of the monocyte-1 chemoattractant protein (MCP-1) [189,190]. In addition, oxLDLs were able to induce cardiac differentiation of cultured MSCs via activation of ERK1/2 signaling pathway [191]. Interestingly, MSCs interfere with a number of atherogenic and cardiotoxic events induced by oxLDLs.…”

Section: Signaling Of Oxldls To Stem Cellsmentioning

confidence: 99%

Oxidized LDLs as Signaling Molecules

2021

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Levels of oxidized low-density lipoproteins (oxLDLs) are usually low in vivo but can increase whenever the balance between formation and scavenging of free radicals is impaired. Under normal conditions, uptake and degradation represent the physiological cellular response to oxLDL exposure. The uptake of oxLDLs is mediated by cell surface scavenger receptors that may also act as signaling molecules. Under conditions of atherosclerosis, monocytes/macrophages and vascular smooth muscle cells highly exposed to oxLDLs tend to convert to foam cells due to the intracellular accumulation of lipids. Moreover, the atherogenic process is accelerated by the increased expression of the scavenger receptors CD36, SR-BI, LOX-1, and SRA in response to high levels of oxLDL and oxidized lipids. In some respects, the effects of oxLDLs, involving cell proliferation, inflammation, apoptosis, adhesion, migration, senescence, and gene expression, can be seen as an adaptive response to the rise of free radicals in the vascular system. Unlike highly reactive radicals, circulating oxLDLs may signal to cells at more distant sites and possibly trigger a systemic antioxidant defense, thus elevating the role of oxLDLs to that of signaling molecules with physiological relevance.

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“…The following supporting information can be downloaded at, Table S1: TLR4 ligands and their possible expression in the bone marrow, effects on bone marrow stromal cells and possible relevance for regulation of hematopoiesis [ 16 , 129 , 130 , 131 , 132 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 , 144 , 145 , 146 , 147 , 148 , 149 , 150 , 151 , 152 , 153 , 154 , 155 , 156 , 157 , 158 , 159 , 160 , 161 , 162 , 163 ], Table S2: A summary of important TLR4 characteristics [ 8 , 17 , 18 , 19 ].…”

mentioning

confidence: 99%

Toll-like Receptor 4, Osteoblasts and Leukemogenesis; the Lesson from Acute Myeloid Leukemia

2022

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Toll-like receptor 4 (TLR4) is a pattern-recognizing receptor that can bind exogenous and endogenous ligands. It is expressed by acute myeloid leukemia (AML) cells, several bone marrow stromal cells, and nonleukemic cells involved in inflammation. TLR4 can bind a wide range of endogenous ligands that are present in the bone marrow microenvironment. Furthermore, the TLR4-expressing nonleukemic bone marrow cells include various mesenchymal cells, endothelial cells, differentiated myeloid cells, and inflammatory/immunocompetent cells. Osteoblasts are important stem cell supporting cells localized to the stem cell niches, and they support the proliferation and survival of primary AML cells. These supporting effects are mediated by the bidirectional crosstalk between AML cells and supportive osteoblasts through the local cytokine network. Finally, TLR4 is also important for the defense against complicating infections in neutropenic patients, and it seems to be involved in the regulation of inflammatory and immunological reactions in patients treated with allogeneic stem cell transplantation. Thus, TLR4 has direct effects on primary AML cells, and it has indirect effects on the leukemic cells through modulation of their supporting neighboring bone marrow stromal cells (i.e., modulation of stem cell niches, regulation of angiogenesis). Furthermore, in allotransplant recipients TLR4 can modulate inflammatory and potentially antileukemic immune reactivity. The use of TLR4 targeting as an antileukemic treatment will therefore depend both on the biology of the AML cells, the biological context of the AML cells, aging effects reflected both in the AML and the stromal cells and the additional antileukemic treatment combined with HSP90 inhibition.

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Oxidized low‐density lipoprotein (ox‐LDL) promotes cardiac differentiation of bone marrow mesenchymal stem cells via activating ERK1/2 signaling

Abstract: Ox-LDL induces cardiac differentiation of BM-MSCs via activation of ERK1/2 signaling.

Cited by 5 publications

References 24 publications

Effect of CD44 on differentiation of human amniotic mesenchymal stem cells into chondrocytes via Smad and ERK signaling pathways

Effect of CD44 on differentiation of human amniotic mesenchymal stem cells into chondrocytes via Smad and ERK signaling pathways

Oxidized LDLs as Signaling Molecules

Toll-like Receptor 4, Osteoblasts and Leukemogenesis; the Lesson from Acute Myeloid Leukemia

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