CD200Fc attenuates inflammatory responses and maintains barrier function by suppressing NF-κB pathway in cigarette smoke extract induced endothelial cells - 03/01/17
, Shihai Shen a, ⁎ Benvenuto su EM|consulte, il riferimento dei professionisti della salute.
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Abstract |
Background |
Recent evidence suggests that CD200 fusion protein (CD200Fc), a CD200R1 agonist may attenuate inflammatory responses in autoimmune diseases and neuro-degeneration. While, little is known about the function of CD200Fc in cigarette smoke extract (CSE)-induced mouse Cardiac Microvascular Endothelial Cells (mCMECs). The present study was designed to elucidate the effects of CD200Fc on CSE-induced vascular endothelial barrier (VEB) dysfunction and inflammatory responses, which is a highly clinically relevant model of smoking related cardiovascular diseases.
Methods |
mCMECs were pre-treated with 1, 10 and 100 μg/ml CD200Fc for 24 h respectively, and then treated with 250 μg/ml CSE for different times (24 h or 120 min). The transepithelial electrical resistance (TEER) and transport of fluorescent markers were used to measure VEB function in CSE-induced mCMECs. Western blot and immunofluorescent staining analysis were used to detect the expression of tight junction proteins, such as Zona Occludens-1 (ZO-1) and Claudin-1 in CSE-induced mCMECs. We measured the expression of pro-inflammatory cytokines in CSE-induced mCMECs by using ELISA and RT-PCR. In addition, the NF-κB activity in CSE-induced mCMECs were investigated by using nuclear/cytosol fractionation and western blot analysis.
Results |
In vitro treatment with CSE increased the transport of fluorescent markers and decreased TEER levels in mCMECs, respectively, which were attenuated by CD200Fc (10 and 100 μg/ml) pretreatment. The CSE-induced up-regulation of pro-inflammatory cytokines such as Cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), platelet endothelial cell adhesion molecule-1 (PECAM-1), vascular cell adhesion molecule-1 (ICAM-1), Prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-8 in mCMECs was also abrogated by CD200Fc (10 and 100 μg/ml) pretreatment. CD200Fc also inhibited CSE-induced nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation in mCMECs, such as inhibition of its DNA binding activity, phosphorylated expression, and translocation to nucleus.
Conclusion |
Thus, CD200Fc exert anti-inflammatory effect and protect VEB function in CSE-induced mCMECs. The vasoprotective effects of CD200Fc may be specifically beneficial in pathophysiological conditions associated with smoking related cardiovascular diseases.
Il testo completo di questo articolo è disponibile in PDF.Keywords : CD200Fc, Inflammatory responses, Vascular endothelial barrier, Cigarette smoke extract, NF-κB pathway, Mouse cardiac microvascular endothelial cells
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Vol 84
P. 714-721 - dicembre 2016 Ritorno al numero
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