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Search results for: CX40

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#33574766   2021/01/26 To Up

Low-Level Vagus Nerve Stimulation Reverses Obstructive Sleep Apnea-Related Atrial Fibrillation by Ameliorating Sympathetic Hyperactivity and Atrial Myocyte Injury.

: Previous studies have proved that low-level vagus nerve stimulation (LLVS) could suppress acute obstructive sleep apnea (OSA), which is associated with atrial fibrillation (AF). : This study investigates the underlying electrophysiological, neural, and cardiomyocyte injury mechanisms on acute OSA-induced AF, examining whether LLVS can attenuate or reverse this remodeling. : Eighteen mongrel dogs received endotracheal intubation under general anesthesia and were randomly divided into three groups: the OSA group (simulated OSA with clamping of the trachea cannula at the end of expiration for 2min followed ventilation 8min, lasting 6h, =6), the OSA+LLVS group (simulated OSA plus LLVS, =6), and a control group (sham clamping the trachea cannula without stimulation, =6). In the OSA+LLVS group, the atrial effective refractory period was significantly lengthened while the sinus node recovery time and AF duration decreased after the 4th hour, and the expression level of Cx40 and Cx43 was significantly increased compared to the OSA group. Norepinephrine, TH, and ChAT were significantly decreased in the OSA+LLVS group compared with the OSA group. Mitochondrial swelling, cardiomyocyte apoptosis, and glycogen deposition, along with a higher concentration of TNF-α, IL-6 were observed in the OSA group, and the LLVS inhibited the structural remodeling and expression of inflammatory cytokines. : LLVS decreased the inducibility of AF partly by ameliorating sympathetic hyperactivity and atrial myocyte injury after acute OSA-induced AF.
Yankai Guo, Jiasuoer Xiaokereti, Qingjun Meng, Guiqiu Cao, Huaxin Sun, Xianhui Zhou, Ling Zhang, Baopeng Tang

1955 related Products with: Low-Level Vagus Nerve Stimulation Reverses Obstructive Sleep Apnea-Related Atrial Fibrillation by Ameliorating Sympathetic Hyperactivity and Atrial Myocyte Injury.

1 mg1 mg100 1 mg5x96 well plate100 1 mg1x96 well plate1000 tests100ul1 ml 6 ml Ready-to-use

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#33525532   2021/01/28 To Up

Alteration of Cx37, Cx40, Cx43, Cx45, Panx1, and Renin Expression Patterns in Postnatal Kidneys of Dab1-/- () Mice.

Numerous evidence corroborates roles of gap junctions/hemichannels in proper kidney development. We analyzed how Dab1 gene functional silencing influences expression and localization of Cx37, Cx40, Cx43, Cx45, Panx1 and renin in postnatal kidneys of mice, by using immunohistochemistry and electron microscopy. Dab1 Δ102/221 might lead to the activation of c-Src tyrosine kinase, causing the upregulation of Cx43 in the medulla of mice. The expression of renin was more prominent in mice ( < 0.001). Renin granules were unusually present inside the vascular walls of glomeruli capillaries, in proximal and distal convoluted tubules and in the medulla. Disfunction of Cx40 is likely responsible for increased atypically positioned renin cells which release renin in an uncontrolled fashion, but this doesn't rule out simultaneous involvement of other Cxs, such as Cx45 which was significantly increased in the cortex. The decreased Cx37 expression in medulla might contribute to hypertension reduction provoked by high renin expression. These findings imply the relevance of Cxs/Panx1 as markers of impaired kidney function (high renin) in mice and that they have a role in the preservation of intercellular signaling and implicate connexopathies as the cause of premature death of mice.
Mirela Lozić, Natalija Filipović, Marija Jurić, Ivona Kosović, Benjamin Benzon, Ivana Šolić, Nela Kelam, Anita Racetin, Koichiro Watanabe, Yu Katsuyama, Masaki Ogata, Mirna Saraga-Babić, Katarina Vukojević

2074 related Products with: Alteration of Cx37, Cx40, Cx43, Cx45, Panx1, and Renin Expression Patterns in Postnatal Kidneys of Dab1-/- () Mice.

5 G300 units100 μg1 Set100 μg1 Set100 μg2ug

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#33429106   2021/01/09 To Up

Connexin45 (GJC1) loss-of-function mutation contributes to familial atrial fibrillation and conduction disease.

Atrial fibrillation (AF) represents the most common clinical cardiac arrhythmia and substantially increases the risk of cerebral stroke, heart failure, and death. Although causative genes for AF have been identified, the genetic determinants for AF remain largely unclear.
Ruo-Gu Li, Ying-Jia Xu, Willy G Ye, Yan-Jie Li, Honghong Chen, Xing-Biao Qiu, Yi-Qing Yang, Donglin Bai

1870 related Products with: Connexin45 (GJC1) loss-of-function mutation contributes to familial atrial fibrillation and conduction disease.

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#33424626   2020/12/23 To Up

Endothelium-Derived Hyperpolarizing Factor and Myoendothelial Coupling: The Perspective.

The endothelium controls vascular tone adopting blood flow to tissue needs. It releases chemical mediators [e.g., nitric oxide (NO), prostaglandins (PG)] and exerts appreciable dilation through smooth muscle hyperpolarization, thus termed endothelium-dependent hyperpolarization (EDH). Initially, EDH was attributed to release of a factor, but later it was suggested that smooth muscle hyperpolarization might be derived from radial spread of an initial endothelial hyperpolarization through heterocellular channels coupling these vascular cells. The channels are indeed present and formed by connexins that enrich in gap junctions (GJ). data suggest that myoendothelial coupling underlies EDH-type dilations as evidenced by blocking experiments as well as simultaneous, merely identical membrane potential changes in endothelial and smooth muscle cells (SMCs), which is indicative of coupling through ohmic resistors. However, connexin-deficient animals do not display any attenuation of EDH-type dilations , and endothelial and SMCs exhibit distinct and barely superimposable membrane potential changes exerted by different means . Even if studied in the exact same artery EDH-type dilation exhibits distinct features and : in isometrically mounted vessels, it is rather weak and depends on myoendothelial coupling through connexin40 (Cx40), whereas as well as under isobaric conditions it is powerful and independent of myoendothelial coupling through Cx40. It is concluded that EDH-type dilations are distinct and a significant dependence on myoendothelial coupling does not reflect the situation under physiologic conditions . Myoendothelial coupling may act as a backup mechanism that is uncovered in the absence of the powerful EDH-type response and possibly reflects a situation in a pathophysiologic environment.
Kjestine Schmidt, Cor de Wit

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#33307937   2020/12/12 To Up

Chronic Hypoxia Decreases Endothelial Connexin 40, Attenuates Endothelium-Dependent Hyperpolarization-Mediated Relaxation in Small Distal Pulmonary Arteries, and Leads to Pulmonary Hypertension.

Background Abnormal endothelial function in the lungs is implicated in the development of pulmonary hypertension; however, there is little information about the difference of endothelial function between small distal pulmonary artery (PA) and large proximal PA and their contribution to the development of pulmonary hypertension. Herein, we investigate endothelium-dependent relaxation in different orders of PAs and examine the molecular mechanisms by which chronic hypoxia attenuates endothelium-dependent pulmonary vasodilation, leading to pulmonary hypertension. Methods and Results Endothelium-dependent relaxation in large proximal PAs (second order) was primarily caused by releasing NO from the endothelium, whereas endothelium-dependent hyperpolarization (EDH)-mediated vasodilation was prominent in small distal PAs (fourth-fifth order). Chronic hypoxia abolished EDH-mediated relaxation in small distal PAs without affecting smooth muscle-dependent relaxation. RNA-sequencing data revealed that, among genes related to EDH, the levels of , , , and were altered in mouse pulmonary endothelial cells isolated from chronically hypoxic mice in comparison to mouse pulmonary endothelial cells from normoxic control mice. The protein levels were significantly lower for connexin 40 (Cx40) and higher for connexin 37 in mouse pulmonary endothelial cells from hypoxic mice than normoxic mice. Cx40 knockout mice exhibited significant attenuation of EDH-mediated relaxation and marked increase in right ventricular systolic pressure. Interestingly, chronic hypoxia led to a further increase in right ventricular systolic pressure in Cx40 knockout mice without altering EDH-mediated relaxation. Furthermore, overexpression of Cx40 significantly decreased right ventricular systolic pressure in chronically hypoxic mice. Conclusions These data suggest that chronic hypoxia-induced downregulation of endothelial Cx40 results in impaired EDH-mediated relaxation in small distal PAs and contributes to the development of pulmonary hypertension.
Rui Si, Qian Zhang, Jody Tori O Cabrera, Qiuyu Zheng, Atsumi Tsuji-Hosokawa, Makiko Watanabe, Susumu Hosokawa, Mingmei Xiong, Pritesh P Jain, Anthony W Ashton, Jason X-J Yuan, Jian Wang, Ayako Makino

2021 related Products with: Chronic Hypoxia Decreases Endothelial Connexin 40, Attenuates Endothelium-Dependent Hyperpolarization-Mediated Relaxation in Small Distal Pulmonary Arteries, and Leads to Pulmonary Hypertension.

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#33172216   2020/11/06 To Up

Connexin Signaling in the Juxtaglomerular Apparatus (JGA) of Developing, Postnatal Healthy and Nephrotic Human Kidneys.

Our study analyzed the expression pattern of different connexins (Cxs) and renin positive cells in the juxtaglomerular apparatus (JGA) of developing, postnatal healthy human kidneys and in nephrotic syndrome of the Finnish type (CNF), by using double immunofluorescence, electron microscopy and statistical measuring. The JGA contained several cell types connected by Cxs, and consisting of macula densa, extraglomerular mesangium (EM) and juxtaglomerular cells (JC), which release renin involved in renin-angiotensin- aldosteron system (RAS) of arterial blood pressure control. During JGA development, strong Cx40 expression gradually decreased, while expression of Cx37, Cx43 and Cx45 increased, postnatally showing more equalized expression patterning. In parallel, initially dispersed renin cells localized to JGA, and greatly increased expression in postnatal kidneys. In CNF kidneys, increased levels of Cx43, Cx37 and Cx45 co-localized with accumulations of renin cells in JGA. Additionally, they reappeared in extraglomerular mesangial cells, indicating association between return to embryonic Cxs patterning and pathologically changed kidney tissue. Based on the described Cxs and renin expression patterning, we suggest involvement of Cx40 primarily in the formation of JGA in developing kidneys, while Cx37, Cx43 and Cx45 might participate in JGA signal transfer important for postnatal maintenance of kidney function and blood pressure control.
Ivona Kosovic, Natalija Filipovic, Benjamin Benzon, Ivana Bocina, Merica Glavina Durdov, Katarina Vukojevic, Marijan Saraga, Mirna Saraga-Babic

1318 related Products with: Connexin Signaling in the Juxtaglomerular Apparatus (JGA) of Developing, Postnatal Healthy and Nephrotic Human Kidneys.

100ul10 100 μg100 μg5108 Sample Kit10ug100 μg0.1 mg100 μg100 μg

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#33163681   2020/11/02 To Up

Regulation of connexins genes expression contributes to reestablishes tissue homeostasis in a renovascular hypertension model.

Connexins (Cx) are essential for cardiovascular regulation and maintenance of cardio-renal response involving the natriuretic peptide family. Changes in the expression of connexins promote intercellular communication dysfunction and may induce hypertension, atherosclerosis, and several other vascular diseases. This study analyzed the expression of the genes involved in the renin-angiotensin system (RAS) and the relation of the connexins gene expression with the renovascular hypertension 2K1C in different tissues. The insertion of a silver clip induced renovascular hypertension 2K1C into the left renal artery. Biochemical measurements were made using commercial kits. Gene expression was evaluated in the liver, heart, and kidneys by RT-PCR. The genes investigated were , r, , , , , , , , , , , and . All genes involved in the RAS presented increased transcriptional levels in the 2K1C group, except hepatic . The natriuretic peptides (; ) and the receptor genes () appeared to increase in the heart, however, Npr1 decreased in the kidneys. In hepatic tissue, hypertension promoted increased expression of 2, , and genes however, and genes were not influenced. Expression was upregulated for and in cardiac tissue in the 2K1C group, but did not demonstrate any difference between groups. The stenotic kidney showed an upregulated expression for vs Sham and contralateral kidney, although and were downregulated. Hypertension did not modify the transcriptional expression of and . Therefore, this study indicated that RAS and cardiac response were regulated transcriptionally by renovascular hypertension 2K1C. Moreover, the results of connexin gene expression demonstrated differential transcriptional regulation in different tissues studied and suggest a relationship between cardiac and renal physiological changes as an adaptive mechanism to the hypertensive state.
Ana Laura Tavares Enes, Caroline Vicente, João Vinicius Grégio, Camila Goulart Clecêncio, Maria Esméria Corezola do Amaral, Camila Andréa de Oliveira

1619 related Products with: Regulation of connexins genes expression contributes to reestablishes tissue homeostasis in a renovascular hypertension model.

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#32984345   2020/08/31 To Up

Gap Junction Dependent Cell Communication Is Modulated During Transdifferentiation of Mesenchymal Stem/Stromal Cells Towards Neuron-Like Cells.

transdifferentiation of patient-derived mesenchymal stem/stromal cells (MSCs) into neurons is of special interest for treatment of neurodegenerative diseases. Although there are encouraging studies, little is known about physiological modulations during this transdifferentiation process. Here, we focus on the analysis of gap junction dependent cell-cell communication and the expression pattern of gap junction-building connexins during small molecule-induced neuronal transdifferentiation of human bone marrow-derived MSCs. During this process, the MSC markers CD73, CD90, CD105, and CD166 were downregulated while the neuronal marker Tuj1 was upregulated. Moreover, the differentiation protocol used in the present study changed the cellular morphology and physiology. The MSCs evolved from a fibroblastoid morphology towards a neuronal shape with round cell bodies and neurite-like processes. Moreover, depolarization evoked action potentials in the transdifferentiated cells. MSCs expressed mRNAs encoding Cx43 and Cx45 as well as trace levels of Cx26, Cx37- and Cx40 and allowed transfer of microinjected Lucifer yellow. The differentiation protocol increased levels of Cx26 (mRNA and protein) and decreased Cx43 (mRNA and protein) while reducing the dye transfer. Cx36 mRNA was nearly undetectable in all cells regardless of treatment. Treatment of the cells with the gap junction coupling inhibitor carbenoxolone (CBX) only modestly altered connexin mRNA levels and had little effect on neuronal differentiation. Our study indicates that the small molecule-based differentiation protocol generates immature neuron-like cells from MSCs. This might be potentially interesting for elucidating physiological modifications and mechanisms in MSCs during the initial steps of differentiation towards a neuronal lineage.
Nadine Dilger, Anna-Lena Neehus, Klaudia Grieger, Andrea Hoffmann, Max Menssen, Anaclet Ngezahayo

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5 x 10A5 cells/vial1 mg11 x 10^6 cells/vial1.5x10(6) cells10 ug0.1ml (1mg/ml)1 vial4 X 250 ml.1 mg10ml1.00 flask

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#32968622   // To Up

Inhibition of ERK or Akt ameliorates intimal hyperplasia via up-regulation of Cx37 and down-regulation of Cx43 in balloon injury rat model.

Connexins (Cxs) are reported to participate in atherosclerosis associated intimal hyperplasia (IH), while their function involved in the balloon injury (BI) induced IH and restenosis is less reported.
Lemen Pan, Haizhen Ni, Wenxu Jin, Xiang Su

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#32923963   2019/11/07 To Up

Endothelial connexins in vascular function.

Gap junctions are essential for intercellular crosstalk in blood and lymphatic vasculature. These clusters of intercellular channels ensure direct communication among endothelial cells and between endothelial and smooth muscle cells, and the synchronization of their behavior along the vascular tree. Gap junction channels are formed by connexins; six connexins form a connexon or hemichannel and the docking of two connexons result in a full gap junction channel allowing for the exchange of ions and small metabolites between neighboring cells. Recent evidence indicates that the intracellular domains of connexins may also function as an interaction platform (interactome) for other proteins, thereby regulating their function. Interestingly, fragments of Cx proteins generated by alternative internal translation were recently described, although their functions in the vascular wall remain to be uncovered. Variations in connexin expression are observed along different types of blood and lymphatic vessels; the most commonly found endothelial connexins are Cx37, Cx40, Cx43 and Cx47. Physiological studies on connexin-knockout mice demonstrated the essential roles of these channel-forming proteins in the coordination of vasomotor activity, endothelial permeability and inflammation, angiogenesis and in the maintenance of fluid balance in the body.
Aurélie Hautefort, Anna Pfenniger, Brenda R Kwak

1599 related Products with: Endothelial connexins in vascular function.

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