2023
DOI: 10.1080/08916934.2023.2200908
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Sema3A inactivates the ERK/JNK signalling pathways to alleviate inflammation and oxidative stress in lipopolysaccharide-stimulated rat endothelial cells and lung tissues

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Cited by 8 publications
(6 citation statements)
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“…In contrast, inhibition of the SEMA3A/NRP-1 complex demonstrated increased production of proinflammatory cytokines and higher mortality [31]. In the transcriptome study (GEO dataset GSE57011), SEMA3A was identified as the most downregulated gene in ARDS patients [20], and overexpression of SEMA3A in the lipopolysaccharides (LPS)-induced ARDS model alleviates oxidative stress and inflammation by suppressing activation of the extracellular signal-regulated kinase/Jun-N-Terminal Kinase (ERK/JNK) signaling pathway in rat pulmonary microvascular endothelial cells [20].…”
Section: Discussionmentioning
confidence: 98%
See 1 more Smart Citation
“…In contrast, inhibition of the SEMA3A/NRP-1 complex demonstrated increased production of proinflammatory cytokines and higher mortality [31]. In the transcriptome study (GEO dataset GSE57011), SEMA3A was identified as the most downregulated gene in ARDS patients [20], and overexpression of SEMA3A in the lipopolysaccharides (LPS)-induced ARDS model alleviates oxidative stress and inflammation by suppressing activation of the extracellular signal-regulated kinase/Jun-N-Terminal Kinase (ERK/JNK) signaling pathway in rat pulmonary microvascular endothelial cells [20].…”
Section: Discussionmentioning
confidence: 98%
“…Studies on mouse models of sepsis showed increased concentrations of several semaphorins in serum and tissues, and a blockade of semaphorins or their receptors led to a reduction in tissue damage and better survival rates [18,19]. In contrast, an experimental study of LPS-induced ARDS revealed decreased SEMA3A concentrations in lung tissue, while SEMA3A overexpression led to less severe lung impairment [20]. Depending on the secreting cells and receptors involved, each SEMA has different and often opposite functions.…”
Section: Introductionmentioning
confidence: 99%
“… 166 In LPS-induced rat pulmonary microvascular endothelial cells (PMVECs) and a rat model of ARDS, overexpression of Sema3A can inhibit the ERK/JNK signaling pathway, thereby improving ECs apoptosis and angiogenesis in the ARDS model, ultimately reducing lung injury and inflammation in rats. 167 …”
Section: The Role Of Endothelial Cells Inflammation In Different Dise...mentioning
confidence: 99%
“…166 In LPS-induced rat pulmonary microvascular endothelial cells (PMVECs) and a rat model of ARDS, overexpression of Sema3A can inhibit the ERK/JNK signaling pathway, thereby improving ECs apoptosis and angiogenesis in the ARDS model, ultimately reducing lung injury and inflammation in rats. 167 In conclusion, this section highlights the unique role of EC inflammation in the pathogenesis of RD. Additionally, we summarize the key signaling pathways that initiate different mechanisms and propagate the inflammatory response, including NF-κB and NLRP3 inflammasome signaling pathways, ERK and STAT3 signaling pathways, PI3K/AKT signaling pathways, Survivin/NF-κB/p65 signaling pathways, ERK/JNK signaling pathway and ROCK2/eNOS signaling pathways.…”
mentioning
confidence: 92%
“…Since then, SEMA3A has been well studied not only in axon guidance, but also in pleiotropic functions, including in angiogenesis, immune cell regulation and cell migration [6]. SEMA3A is expressed in kidneys, as well as the nervous system, heart, lung, eyes, bone and immune cells [7][8][9][10][11][12], and regulates tissue development and the maintenance of homeostasis, for example, through the regulation of cell proliferation and migration, and the immune system [13][14][15]. Several reports have identified an increase or decrease in SEMA3A expression under several disease conditions [16][17][18][19]; thus, SEMA3A has been suggested as a possible biomarker, as well as a therapeutic target.…”
Section: Introductionmentioning
confidence: 99%