Malat1 long noncoding RNA regulates inflammation and leukocyte differentiation in experimental autoimmune encephalomyelitis

The implication of circulating long non-coding RNA MALAT1 in diagnosis, disease surveillance and prognosis of acute ischemic stroke

“…[12] Considering that lnc-MALAT1 might participate in the cerebrovascular pathologies of stroke according to previous studies, meanwhile, it presented anti-inflammatory effect in cardiovascular and cerebrovascular diseases, we hypothesized that lnc-MALAT1 expression might be related to the disease risk, progression or inflammation level of AIS, while related explorations in AIS are seldomly reported. [9][10][11][12]23] In our study, we assessed the predictive value of lnc-MALAT1 for AIS risk, and we discovered that lnc-MALAT1 expression was lower in AIS patients compared to controls, and lnc-MALAT1 expression presented good diagnostic value for AIS, which might due to its protective effect in these diseases via repressing cell apoptosis of BMECs. Moreover, we investigated the correlation of lnc-MALAT1 expression with disease severity as well as inflammation in AIS patients, and we observed that lnc-MALAT1 high expression was associated with decreased NIHSS score, reduced levels of inflammatory factors (including CRP, TNF-α, IL-6, IL-8 and IL-22), meanwhile it reduced proportion of diabetes but numerically increased proportion of hypertension (without significant difference) in AIS patients.…”

“…[7] As to its role in neurological diseases or cerebrovascular diseases, previous studies demonstrate that lnc-MALAT1 has protective effects in these diseases via repressing proapoptotic or pro-inflammatory factors. [10,11,18,19] For instance, a study displays that lnc-MALAT1 protects human brain vascular endothelial cells from OGD-induced apoptosis through activating phosphatidylinositol 3-kinase (PI3K). [19] In addition, lnc-MALAT1 expression is decreased in the spinal cords of mice with experimental autoimmune encephalomyelitis, and its knockdown raises levels of inflammatory cytokines (including IL-1 and IL-6).…”

“…[19] In addition, lnc-MALAT1 expression is decreased in the spinal cords of mice with experimental autoimmune encephalomyelitis, and its knockdown raises levels of inflammatory cytokines (including IL-1 and IL-6). [11] Also, silencing of lnc-MALAT1 raises the levels of proapoptotic factor Bim and proinflammatory cytokines (including MCP-1 as well as E-selectin) in BMECs following oxygen-glucose deprivation (OGD), which is an in vitro mimic of ischemic stroke conditions. [10] Another study discloses that lnc-MALAT1 knockdown aggravates OGD-induced overexpression of pro-inflammatory cytokines including MCP-1 and IL-6 in mouse cerebral microvascular endothelial cells.…”

“…[20][21][22] Just a few studies display that lnc-MALAT1 expression is reduced in central nervous system tissues from multiple sclerosis patients and carotid plaques from atherosclerosis patients. [11,12] As for the correlation of lnc-MALAT1 with disease severity and inflammation in neurological diseases or cerebrovascular diseases patients, only a study shows that elevated lnc-MALAT1 expression is correlated with less advanced lesions in atherosclerosis patients. [12] Considering that lnc-MALAT1 might participate in the cerebrovascular pathologies of stroke according to previous studies, meanwhile, it presented anti-inflammatory effect in cardiovascular and cerebrovascular diseases, we hypothesized that lnc-MALAT1 expression might be related to the disease risk, progression or inflammation level of AIS, while related explorations in AIS are seldomly reported.…”

“…[9,10] Meanwhile, lnc-MALAT1 has been reported to be downregulated and primarily plays an anti-inflammatory role in neurological diseases patients as well as cardiovascular and cerebrovascular diseases patients. [11,12] Considering the participation of lnc-MALAT1 in cerebrovascular pathologies of stroke and its anti-inflammation effect on cardiovascular and cerebrovascular diseases, we hypothesized that lnc-MALAT1 might serve as a biomarker for disease risk and progression in AIS through affecting inflammation level, whereas related evidences were seldomly reported. Hence, we conducted this study to investigate the predictive value of lnc-MALAT1 for AIS risk, and the association of lnc-MALAT1 expression with disease severity, inflammation level as well as recurrence free survival (RFS) in AIS patients.…”