scholarly journals Paeoniflorin attenuates incipient diabetic nephropathy in streptozotocin-induced mice by the suppression of the Toll-like receptor-2 signaling pathway

2017 ◽  
Vol Volume 11 ◽  
pp. 3221-3233 ◽  
Author(s):  
Yun-xia Shao ◽  
Xing-xin Xu ◽  
Kun Wang ◽  
Xiang-ming Qi ◽  
Yong-gui Wu
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Toll Like Receptor ◽  
Incipient Diabetic Nephropathy ◽  
Toll Like Receptor 2

scholarly journals Knockout of Toll-Like Receptor-2 Attenuates Both the Proinflammatory State of Diabetes and Incipient Diabetic Nephropathy

2011 ◽  
Vol 31 (8) ◽  
pp. 1796-1804 ◽  
Author(s):  
Sridevi Devaraj ◽  
Peter Tobias ◽  
Balakuntalam S. Kasinath ◽  
Rajendra Ramsamooj ◽  
Alaa Afify ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Toll Like Receptor ◽  
Incipient Diabetic Nephropathy ◽  
Toll Like Receptor 2

scholarly journals Toll like receptor 2 signaling pathway in endothelial barrier regulation

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Agnieszka Jezierska‐Drutel ◽  
Irina Kolosova ◽  
Alexander D Verin
Keyword(s):  
Signaling Pathway ◽  
Endothelial Barrier ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Barrier Regulation

Increased Expression of Toll-Like Receptor 2 in Rat Diabetic Nephropathy

2010 ◽  
Vol 32 (2) ◽  
pp. 179-186 ◽  
Author(s):  
Fanglin Li ◽  
Niansheng Yang ◽  
Lili Zhang ◽  
Hechang Tan ◽  
Bin Huang ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

Treponema pallidum flagellin FlaA2 induces IL-6 secretion in THP-1 cells via the Toll-like receptor 2 signaling pathway

2017 ◽  
Vol 81 ◽  
pp. 42-51 ◽  
Author(s):  
Yafeng Xie ◽  
Man Xu ◽  
Yongjian Xiao ◽  
Zhuoran Liu ◽  
Chuanhao Jiang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Treponema Pallidum ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Increasing toll-like receptor 2 on astrocytes induced by Schwann cell-derived exosomes promotes recovery by inhibiting CSPGs deposition after spinal cord injury

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Dayu Pan ◽  
Yongjin Li ◽  
Fuhan Yang ◽  
Zenghui Lv ◽  
Shibo Zhu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Schwann Cell ◽  
Western Blot ◽  
Signaling Pathway ◽  
Functional Recovery ◽  
Toll Like Receptor ◽  
Tlr2 Expression ◽  
Cord Injury ◽  
Toll Like Receptor 2

Abstract Background Traumatic spinal cord injury (SCI) is a severely disabling disease that leads to loss of sensation, motor, and autonomic function. As exosomes have great potential in diagnosis, prognosis, and treatment of SCI because of their ability to easily cross the blood–brain barrier, the function of Schwann cell-derived exosomes (SCDEs) is still largely unknown. Methods A T10 spinal cord contusion was established in adult female mice. SCDEs were injected into the tail veins of mice three times a week for 4 weeks after the induction of SCI, and the control group was injected with PBS. High-resolution transmission electron microscope and western blot were used to characterize the SCDEs. Toll-like receptor 2 (TLR2) expression on astrocytes, chondroitin sulfate proteoglycans (CSPGs) deposition and neurological function recovery were measured in the spinal cord tissues of each group by immunofluorescence staining of TLR2, GFAP, CS56, 5-HT, and β-III-tublin, respectively. TLR2f/f mice were crossed to the GFAP-Cre strain to generate astrocyte specific TLR2 knockout mice (TLR2−/−). Finally, western blot analysis was used to determine the expression of signaling proteins and IKKβ inhibitor SC-514 was used to validate the involved signaling pathway. Results Here, we found that TLR2 increased significantly on astrocytes post-SCI. SCDEs treatment can promote functional recovery and induce the expression of TLR2 on astrocytes accompanied with decreased CSPGs deposition. The specific knockout of TLR2 on astrocytes abolished the decreasing CSPGs deposition and neurological functional recovery post-SCI. In addition, the signaling pathway of NF-κB/PI3K involved in the TLR2 activation was validated by western blot. Furthermore, IKKβ inhibitor SC-514 was also used to validate this signaling pathway. Conclusion Thus, our results uncovered that SCDEs can promote functional recovery of mice post-SCI by decreasing the CSPGs deposition via increasing the TLR2 expression on astrocytes through NF-κB/PI3K signaling pathway.

scholarly journals Chlamydia pneumoniae Infection Promotes Vascular Smooth Muscle Cell Migration through a Toll-Like Receptor 2-Related Signaling Pathway

2013 ◽  
Vol 81 (12) ◽  
pp. 4583-4591 ◽  
Author(s):  
Beibei Wang ◽  
Lijun Zhang ◽  
Tengteng Zhang ◽  
Haiwei Wang ◽  
Junxia Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathway ◽  
Chlamydia Pneumoniae ◽  
Neutralizing Antibody ◽  
Toll Like Receptor ◽  
Rt Pcr ◽  
Content Type ◽  
Akt Phosphorylation ◽  
Toll Like Receptor 2 ◽  
Tlr2 Mrna

ABSTRACTThe migration of vascular smooth muscle cells (VSMCs) from the media to the intima is proposed to be a key event in the development of atherosclerosis. Recently, we reported thatChlamydia pneumoniaeinfection is involved in VSMC migration. However, the exact mechanisms forC. pneumoniaeinfection-induced VSMC migration are not yet well elucidated. In this study, we examined the role of the Toll-like receptor 2 (TLR2) activation-related signaling pathway in VSMC migration induced byC. pneumoniaeinfection. An Affymetrix-based gene expression array was conducted to identify the changes of gene expression in rat primary VSMCs (rVSMCs) infected withC. pneumoniae. Both the microarray analysis and quantitative real-time reverse transcription (RT)-PCR revealed that TLR2 mRNA expression was strongly upregulated 12 h afterC. pneumoniaeinfection. RT-PCR and Western blot analysis further showed that the expression levels of TLR2 mRNA and protein significantly increased at the different time points after infection. Immunocytochemical analysis suggested a TLR2 recruitment to the vicinity ofC. pneumoniaeinclusions. Cell migration assays showed that the TLR2-neutralizing antibody could significantly inhibitC. pneumoniaeinfection-induced rVSMC migration. In addition,C. pneumoniaeinfection stimulated Akt phosphorylation at Ser 473, which was obviously suppressed by the PI3K inhibitor LY294002, thereby inhibiting rVSMC migration caused byC. pneumoniaeinfection. Furthermore, both the infection-induced Akt phosphorylation and rVSMC migration were suppressed by the TLR2-neutralizing antibody. Taken together, these data suggest thatC. pneumoniaeinfection can promote VSMC migration possibly through the TLR2-related signaling pathway.

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