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

Qiu, Qianwen; Yu, Xuezhong; Chen, Qingli; He, Xuwei

doi:10.1080/08916934.2023.2200908

Cited by 6 publications

(6 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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%

See 1 more Smart Citation

Association of Immune Semaphorins with COVID-19 Severity and Outcomes

Vargovic,

Papic,

Samadan

et al. 2023

Biomedicines

View full text Add to dashboard Cite

Semaphorins have recently been recognized as crucial modulators of immune responses. In the pathogenesis of COVID-19, the activation of immune responses is the key factor in the development of severe disease. This study aimed to determine the association of serum semaphorin concentrations with COVID-19 severity and outcomes. Serum semaphorin concentrations (SEMA3A, -3C, -3F, -4D, -7A) were measured in 80 hospitalized adult patients with COVID-19 (moderate (n = 24), severe (n = 32), critical, (n = 24)) and 40 healthy controls. While SEMA3C, SEMA3F and SEMA7A serum concentrations were significantly higher in patients with COVID-19, SEMA3A was significantly lower. Furthermore, SEMA3A and SEMA3C decreased with COVID-19 severity, while SEMA3F and SEMA7A increased. SEMA4D showed no correlation with disease severity. Serum semaphorin levels show better predictive values than CRP, IL-6 and LDH for differentiating critical from moderate/severe COVID-19. SEMA3F and SEMA7A serum concentrations were associated with the time to recovery, requirement of invasive mechanical ventilation, development of pulmonary thrombosis and nosocomial infections, as well as with in-hospital mortality. In conclusion, we provide the first evidence that SEMA3A, SEMA3C, SEMA3F and SEMA7A can be considered as new biomarkers of COVID-19 severity.

show abstract

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Association of Immune Semaphorins with COVID-19 Severity and Outcomes

Vargovic,

Papic,

Samadan

et al. 2023

Biomedicines

View full text Add to dashboard Cite

show abstract

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%

Research Progress and Molecular Mechanisms of Endothelial Cells Inflammation in Vascular-Related Diseases

Xue,

Zhang,

Sun

et al. 2023

JIR

View full text Add to dashboard Cite

Endothelial cells (ECs) are widely distributed inside the vascular network, forming a vital barrier between the bloodstream and the walls of blood vessels. These versatile cells serve myriad functions, including the regulation of vascular tension and the management of hemostasis and thrombosis. Inflammation constitutes a cascade of biological responses incited by biological, chemical, or physical stimuli. While inflammation is inherently a protective mechanism, dysregulated inflammation can precipitate a host of vascular pathologies. ECs play a critical role in the genesis and progression of vascular inflammation, which has been implicated in the etiology of numerous vascular disorders, such as atherosclerosis, cardiovascular diseases, respiratory diseases, diabetes mellitus, and sepsis. Upon activation, ECs secrete potent inflammatory mediators that elicit both innate and adaptive immune reactions, culminating in inflammation. To date, no comprehensive and nuanced account of the research progress concerning ECs and inflammation in vascular-related maladies exists. Consequently, this review endeavors to synthesize the contributions of ECs to inflammatory processes, delineate the molecular signaling pathways involved in regulation, and categorize and consolidate the various models and treatment strategies for vascular-related diseases. It is our aspiration that this review furnishes cogent experimental evidence supporting the established link between endothelial inflammation and vascular-related pathologies, offers a theoretical foundation for clinical investigations, and imparts valuable insights for the development of therapeutic agents targeting these diseases.

show abstract

“…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%

Role of Semaphorin 3A in Kidney Development and Diseases

Sang,

Tsuji,

Nakanoh

et al. 2023

Diagnostics

View full text Add to dashboard Cite

Kidney diseases are worldwide public health problems affecting millions of people. However, there are still limited therapeutic options against kidney diseases. Semaphorin 3A (SEMA3A) is a secreted and membrane-associated protein, which regulates diverse functions, including immune regulation, cell survival, migration and angiogenesis, thus involving in the several pathogeneses of diseases, including eyes and neurons, as well as kidneys. SEMA3A is expressed in podocytes and tubular cells in the normal adult kidney, and recent evidence has revealed that excess SEMA3A expression and the subsequent signaling pathway aggravate kidney injury in a variety of kidney diseases, including nephrotic syndrome, diabetic nephropathy, acute kidney injury, and chronic kidney disease. In addition, several reports have demonstrated that the inhibition of SEMA3A ameliorated kidney injury via a reduction in cell apoptosis, fibrosis and inflammation; thus, SEMA3A may be a potential therapeutic target for kidney diseases. In this review article, we summarized the current knowledge regarding the role of SEMA3A in kidney pathophysiology and their potential use in kidney diseases.

show abstract

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

Cited by 6 publications

References 35 publications

Association of Immune Semaphorins with COVID-19 Severity and Outcomes

Association of Immune Semaphorins with COVID-19 Severity and Outcomes

Research Progress and Molecular Mechanisms of Endothelial Cells Inflammation in Vascular-Related Diseases

Role of Semaphorin 3A in Kidney Development and Diseases

Contact Info

Product

Resources

About