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Attenuated platelet aggregation in patients with septic shock is independent from the activity state of myosin light chain phosphorylation or a reduction in Rho kinase-dependent inhibition of myosin light chain phosphatase.

Intensive care medicine experimental

Reddi BA, Iannella SM, O'Connor SN, Deane AM, Willoughby SR, Wilson DP.
PMID: 26215804
Intensive Care Med Exp. 2015 Dec;3(1):37. doi: 10.1186/s40635-014-0037-7. Epub 2015 Feb 12.

BACKGROUND: Impaired coagulation contributes to the morbidity and mortality associated with septic shock. Whether abnormal platelet contraction adds to the bleeding tendency is unknown. Platelets contract when Ca(2+)-dependent myosin light chain kinase (MLCK) phosphorylates Ser19 of myosin light chain...

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Reddi BA, Iannella SM, O'Connor SN, et al. Attenuated platelet aggregation in patients with septic shock is independent from the activity state of myosin light chain phosphorylation or a reduction in Rho kinase-dependent inhibition of myosin light chain phosphatase. Intensive Care Med Exp. 2015;3(1):37doi: 10.1186/s40635-014-0037-7.
Reddi, B. A., Iannella, S. M., O'Connor, S. N., Deane, A. M., Willoughby, S. R., & Wilson, D. P. (2015). Attenuated platelet aggregation in patients with septic shock is independent from the activity state of myosin light chain phosphorylation or a reduction in Rho kinase-dependent inhibition of myosin light chain phosphatase. Intensive care medicine experimental, 3(1), 37. https://doi.org/10.1186/s40635-014-0037-7
Reddi, Benjamin Aj, et al. "Attenuated platelet aggregation in patients with septic shock is independent from the activity state of myosin light chain phosphorylation or a reduction in Rho kinase-dependent inhibition of myosin light chain phosphatase." Intensive care medicine experimental vol. 3,1 (2015): 37. doi: https://doi.org/10.1186/s40635-014-0037-7
Reddi BA, Iannella SM, O'Connor SN, Deane AM, Willoughby SR, Wilson DP. Attenuated platelet aggregation in patients with septic shock is independent from the activity state of myosin light chain phosphorylation or a reduction in Rho kinase-dependent inhibition of myosin light chain phosphatase. Intensive Care Med Exp. 2015 Dec;3(1):37. doi: 10.1186/s40635-014-0037-7. Epub 2015 Feb 12. PMID: 26215804; PMCID: PMC4512995.
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Phorbol 12,13-dibutyrate-induced, protein kinase C-mediated contraction of rabbit bladder smooth muscle.

Frontiers in pharmacology

Wang T, Kendig DM, Trappanese DM, Smolock EM, Moreland RS.
PMID: 22232602
Front Pharmacol. 2012 Jan 02;2:83. doi: 10.3389/fphar.2011.00083. eCollection 2012.

Contraction of bladder smooth muscle is predominantly initiated by M(3) muscarinic receptor-mediated activation of the G(q/11)-phospholipase C β-protein kinase C (PKC) and the G(12/13)-RhoGEF-Rho kinase (ROCK) pathways. However, these pathways and their downstream effectors are not well understood in...

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Wang T, Kendig DM, Trappanese DM, et al. Phorbol 12,13-dibutyrate-induced, protein kinase C-mediated contraction of rabbit bladder smooth muscle. Front Pharmacol. 2012;2:83doi: 10.3389/fphar.2011.00083.
Wang, T., Kendig, D. M., Trappanese, D. M., Smolock, E. M., & Moreland, R. S. (2012). Phorbol 12,13-dibutyrate-induced, protein kinase C-mediated contraction of rabbit bladder smooth muscle. Frontiers in pharmacology, 283. https://doi.org/10.3389/fphar.2011.00083
Wang, Tanchun, et al. "Phorbol 12,13-dibutyrate-induced, protein kinase C-mediated contraction of rabbit bladder smooth muscle." Frontiers in pharmacology vol. 2 (2012): 83. doi: https://doi.org/10.3389/fphar.2011.00083
Wang T, Kendig DM, Trappanese DM, Smolock EM, Moreland RS. Phorbol 12,13-dibutyrate-induced, protein kinase C-mediated contraction of rabbit bladder smooth muscle. Front Pharmacol. 2012 Jan 02;2:83. doi: 10.3389/fphar.2011.00083. eCollection 2012. PMID: 22232602; PMCID: PMC3249380.
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Regulation of Myosin Light-Chain Phosphatase Activity to Generate Airway Smooth Muscle Hypercontractility.

Frontiers in physiology

Álvarez-Santos MD, Álvarez-González M, Estrada-Soto S, Bazán-Perkins B.
PMID: 32676037
Front Physiol. 2020 Jun 26;11:701. doi: 10.3389/fphys.2020.00701. eCollection 2020.

Smooth muscle is a central structure involved in the regulation of airway tone. In addition, it plays an important role in the development of some pathologies generated by alterations in contraction, such as hypercontractility and the airway hyperresponsiveness observed...

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Álvarez-Santos MD, Álvarez-González M, Estrada-Soto S, et al. Regulation of Myosin Light-Chain Phosphatase Activity to Generate Airway Smooth Muscle Hypercontractility. Front Physiol. 2020;11:701doi: 10.3389/fphys.2020.00701.
Álvarez-Santos, M. D., Álvarez-González, M., Estrada-Soto, S., & Bazán-Perkins, B. (2020). Regulation of Myosin Light-Chain Phosphatase Activity to Generate Airway Smooth Muscle Hypercontractility. Frontiers in physiology, 11701. https://doi.org/10.3389/fphys.2020.00701
Álvarez-Santos, Mayra D, et al. "Regulation of Myosin Light-Chain Phosphatase Activity to Generate Airway Smooth Muscle Hypercontractility." Frontiers in physiology vol. 11 (2020): 701. doi: https://doi.org/10.3389/fphys.2020.00701
Álvarez-Santos MD, Álvarez-González M, Estrada-Soto S, Bazán-Perkins B. Regulation of Myosin Light-Chain Phosphatase Activity to Generate Airway Smooth Muscle Hypercontractility. Front Physiol. 2020 Jun 26;11:701. doi: 10.3389/fphys.2020.00701. eCollection 2020. PMID: 32676037; PMCID: PMC7333668.
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Data for increased Rho kinase activity in type 2 diabetic patients.

Data in brief

Liu L, Tan L, Lai J, Li S, Wang DW.
PMID: 27896306
Data Brief. 2016 Nov 16;9:978-982. doi: 10.1016/j.dib.2016.11.032. eCollection 2016 Dec.

The data presented in this article are related to the research article entitled "Enhanced Rho-Kinase Activity: Pathophysiological Relevance in Type 2 Diabetes" [1]. Rho-Kinase has attracted a great deal of interest as a novel therapeutic target in cardiovascular diseases....

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Liu L, Tan L, Lai J, et al. Data for increased Rho kinase activity in type 2 diabetic patients. Data Brief. 2016;9:978-982doi: 10.1016/j.dib.2016.11.032.
Liu, L., Tan, L., Lai, J., Li, S., & Wang, D. W. (2016). Data for increased Rho kinase activity in type 2 diabetic patients. Data in brief, 9978-982. https://doi.org/10.1016/j.dib.2016.11.032
Liu, Lei, et al. "Data for increased Rho kinase activity in type 2 diabetic patients." Data in brief vol. 9 (2016): 978-982. doi: https://doi.org/10.1016/j.dib.2016.11.032
Liu L, Tan L, Lai J, Li S, Wang DW. Data for increased Rho kinase activity in type 2 diabetic patients. Data Brief. 2016 Nov 16;9:978-982. doi: 10.1016/j.dib.2016.11.032. eCollection 2016 Dec. PMID: 27896306; PMCID: PMC5120266.
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Mfge8 attenuates human gastric antrum smooth muscle contractions.

Journal of muscle research and cell motility

Li W, Olseen A, Xie Y, Alexandru C, Outland A, Herrera AF, Syder AJ, Wykosky J, Perrino BA.
PMID: 34085177
J Muscle Res Cell Motil. 2021 Jun;42(2):219-231. doi: 10.1007/s10974-021-09604-y. Epub 2021 Jun 03.

Coordinated gastric smooth muscle contraction is critical for proper digestion and is adversely affected by a number of gastric motility disorders. In this study we report that the secreted protein Mfge8 (milk fat globule-EGF factor 8) inhibits the contractile...

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Li W, Olseen A, Xie Y, et al. Mfge8 attenuates human gastric antrum smooth muscle contractions. J Muscle Res Cell Motil. 2021;42(2):219-231doi: 10.1007/s10974-021-09604-y.
Li, W., Olseen, A., Xie, Y., Alexandru, C., Outland, A., Herrera, A. F., Syder, A. J., Wykosky, J., & Perrino, B. A. (2021). Mfge8 attenuates human gastric antrum smooth muscle contractions. Journal of muscle research and cell motility, 42(2), 219-231. https://doi.org/10.1007/s10974-021-09604-y
Li, Wen, et al. "Mfge8 attenuates human gastric antrum smooth muscle contractions." Journal of muscle research and cell motility vol. 42,2 (2021): 219-231. doi: https://doi.org/10.1007/s10974-021-09604-y
Li W, Olseen A, Xie Y, Alexandru C, Outland A, Herrera AF, Syder AJ, Wykosky J, Perrino BA. Mfge8 attenuates human gastric antrum smooth muscle contractions. J Muscle Res Cell Motil. 2021 Jun;42(2):219-231. doi: 10.1007/s10974-021-09604-y. Epub 2021 Jun 03. PMID: 34085177; PMCID: PMC8332633.
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TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner.

Acta pharmaceutica Sinica. B

Zheng H, Li X, Zeng X, Huang C, Ma M, Lv X, Zhang Y, Sun L, Wang G, Du Y, Guan Y.
PMID: 35024321
Acta Pharm Sin B. 2021 Dec;11(12):3994-4007. doi: 10.1016/j.apsb.2021.04.013. Epub 2021 Apr 22.

Vascular smooth muscle cell (VSMC) migration plays a critical role in the pathogenesis of many cardiovascular diseases. We recently showed that TMEM16A is involved in hypertension-induced cerebrovascular remodeling. However, it is unclear whether this effect is related to the...

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Zheng H, Li X, Zeng X, et al. TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner. Acta Pharm Sin B. 2021;11(12):3994-4007doi: 10.1016/j.apsb.2021.04.013.
Zheng, H., Li, X., Zeng, X., Huang, C., Ma, M., Lv, X., Zhang, Y., Sun, L., Wang, G., Du, Y., & Guan, Y. (2021). TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner. Acta pharmaceutica Sinica. B, 11(12), 3994-4007. https://doi.org/10.1016/j.apsb.2021.04.013
Zheng, Huaqing, et al. "TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner." Acta pharmaceutica Sinica. B vol. 11,12 (2021): 3994-4007. doi: https://doi.org/10.1016/j.apsb.2021.04.013
Zheng H, Li X, Zeng X, Huang C, Ma M, Lv X, Zhang Y, Sun L, Wang G, Du Y, Guan Y. TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner. Acta Pharm Sin B. 2021 Dec;11(12):3994-4007. doi: 10.1016/j.apsb.2021.04.013. Epub 2021 Apr 22. PMID: 35024321; PMCID: PMC8727780.
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Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction.

Evidence-based complementary and alternative medicine : eCAM

Lin Z, Zhang C, Zhang X, Shi N, Wen Y, Han C, Du D, Liu T, Jin T, Deng L, Jiang K, Yang X, Guo J, Philips A, Sutton R, Windsor JA, Huang W, Xue P, Xia Q.
PMID: 32104199
Evid Based Complement Alternat Med. 2020 Feb 10;2020:9189457. doi: 10.1155/2020/9189457. eCollection 2020.

Protein kinase C-potentiated inhibitor protein of 17 kDa (CPI-17), a specific inhibitor of myosin light-chain phosphatase (MLCP) regulated by proinflammatory cytokines, is central for calcium sensitisation. We investigated the effects of chaiqin chengqi decoction (CQCQD) on the CPI-17/MLCP pathway...

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Lin Z, Zhang C, Zhang X, et al. Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction. Evid Based Complement Alternat Med. 2020;2020:9189457doi: 10.1155/2020/9189457.
Lin, Z., Zhang, C., Zhang, X., Shi, N., Wen, Y., Han, C., Du, D., Liu, T., Jin, T., Deng, L., Jiang, K., Yang, X., Guo, J., Philips, A., Sutton, R., Windsor, J. A., Huang, W., Xue, P., & Xia, Q. (2020). Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction. Evidence-based complementary and alternative medicine : eCAM, 20209189457. https://doi.org/10.1155/2020/9189457
Lin, Ziqi, et al. "Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction." Evidence-based complementary and alternative medicine : eCAM vol. 2020 (2020): 9189457. doi: https://doi.org/10.1155/2020/9189457
Lin Z, Zhang C, Zhang X, Shi N, Wen Y, Han C, Du D, Liu T, Jin T, Deng L, Jiang K, Yang X, Guo J, Philips A, Sutton R, Windsor JA, Huang W, Xue P, Xia Q. Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction. Evid Based Complement Alternat Med. 2020 Feb 10;2020:9189457. doi: 10.1155/2020/9189457. eCollection 2020. PMID: 32104199; PMCID: PMC7035521.
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Calyculin A, an enhancer of myosin, speeds up anaphase chromosome movement.

Cell & chromosome

Fabian L, Troscianczuk J, Forer A.
PMID: 17381845
Cell Chromosome. 2007 Mar 24;6:1. doi: 10.1186/1475-9268-6-1.

Actin and myosin inhibitors often blocked anaphase movements in insect spermatocytes in previous experiments. Here we treat cells with an enhancer of myosin, Calyculin A, which inhibits myosin-light-chain phosphatase from dephosphorylating myosin; myosin thus is hyperactivated. Calyculin A causes...

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Fabian L, Troscianczuk J, Forer A. Calyculin A, an enhancer of myosin, speeds up anaphase chromosome movement. Cell Chromosome. 2007;6:1doi: 10.1186/1475-9268-6-1.
Fabian, L., Troscianczuk, J., & Forer, A. (2007). Calyculin A, an enhancer of myosin, speeds up anaphase chromosome movement. Cell & chromosome, 61. https://doi.org/10.1186/1475-9268-6-1
Fabian, Lacramioara, et al. "Calyculin A, an enhancer of myosin, speeds up anaphase chromosome movement." Cell & chromosome vol. 6 (2007): 1. doi: https://doi.org/10.1186/1475-9268-6-1
Fabian L, Troscianczuk J, Forer A. Calyculin A, an enhancer of myosin, speeds up anaphase chromosome movement. Cell Chromosome. 2007 Mar 24;6:1. doi: 10.1186/1475-9268-6-1. PMID: 17381845; PMCID: PMC1847834.
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TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner.

Acta pharmaceutica Sinica. B

Zheng H, Li X, Zeng X, Huang C, Ma M, Lv X, Zhang Y, Sun L, Wang G, Du Y, Guan Y.
PMID: 35024321
Acta Pharm Sin B. 2021 Dec;11(12):3994-4007. doi: 10.1016/j.apsb.2021.04.013. Epub 2021 Apr 22.

Vascular smooth muscle cell (VSMC) migration plays a critical role in the pathogenesis of many cardiovascular diseases. We recently showed that TMEM16A is involved in hypertension-induced cerebrovascular remodeling. However, it is unclear whether this effect is related to the...

Cite
Zheng H, Li X, Zeng X, et al. TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner. Acta Pharm Sin B. 2021;11(12):3994-4007doi: 10.1016/j.apsb.2021.04.013.
Zheng, H., Li, X., Zeng, X., Huang, C., Ma, M., Lv, X., Zhang, Y., Sun, L., Wang, G., Du, Y., & Guan, Y. (2021). TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner. Acta pharmaceutica Sinica. B, 11(12), 3994-4007. https://doi.org/10.1016/j.apsb.2021.04.013
Zheng, Huaqing, et al. "TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner." Acta pharmaceutica Sinica. B vol. 11,12 (2021): 3994-4007. doi: https://doi.org/10.1016/j.apsb.2021.04.013
Zheng H, Li X, Zeng X, Huang C, Ma M, Lv X, Zhang Y, Sun L, Wang G, Du Y, Guan Y. TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner. Acta Pharm Sin B. 2021 Dec;11(12):3994-4007. doi: 10.1016/j.apsb.2021.04.013. Epub 2021 Apr 22. PMID: 35024321; PMCID: PMC8727780.
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Orthovanadate-induced vasocontraction is mediated by the activation of Rho-kinase through Src-dependent transactivation of epidermal growth factor receptor.

Pharmacology research & perspectives

Yayama K, Sasahara T, Ohba H, Funasaka A, Okamoto H.
PMID: 25505586
Pharmacol Res Perspect. 2014 Apr;2(2):e00039. doi: 10.1002/prp2.39. Epub 2014 Apr 01.

Orthovanadate (OVA), a protein tyrosine phosphatase (PTPase) inhibitor, exerts contractile effects on smooth muscle in a Rho-kinase-dependent manner, but the precise mechanisms are not elucidated. The aim of this study was to determine the potential roles of Src and...

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Yayama K, Sasahara T, Ohba H, et al. Orthovanadate-induced vasocontraction is mediated by the activation of Rho-kinase through Src-dependent transactivation of epidermal growth factor receptor. Pharmacol Res Perspect. 2014;2(2):e00039doi: 10.1002/prp2.39.
Yayama, K., Sasahara, T., Ohba, H., Funasaka, A., & Okamoto, H. (2014). Orthovanadate-induced vasocontraction is mediated by the activation of Rho-kinase through Src-dependent transactivation of epidermal growth factor receptor. Pharmacology research & perspectives, 2(2), e00039. https://doi.org/10.1002/prp2.39
Yayama, Katsutoshi, et al. "Orthovanadate-induced vasocontraction is mediated by the activation of Rho-kinase through Src-dependent transactivation of epidermal growth factor receptor." Pharmacology research & perspectives vol. 2,2 (2014): e00039. doi: https://doi.org/10.1002/prp2.39
Yayama K, Sasahara T, Ohba H, Funasaka A, Okamoto H. Orthovanadate-induced vasocontraction is mediated by the activation of Rho-kinase through Src-dependent transactivation of epidermal growth factor receptor. Pharmacol Res Perspect. 2014 Apr;2(2):e00039. doi: 10.1002/prp2.39. Epub 2014 Apr 01. PMID: 25505586; PMCID: PMC4184709.
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TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner.

Acta pharmaceutica Sinica. B

Zheng H, Li X, Zeng X, Huang C, Ma M, Lv X, Zhang Y, Sun L, Wang G, Du Y, Guan Y.
PMID: 35024321
Acta Pharm Sin B. 2021 Dec;11(12):3994-4007. doi: 10.1016/j.apsb.2021.04.013. Epub 2021 Apr 22.

Vascular smooth muscle cell (VSMC) migration plays a critical role in the pathogenesis of many cardiovascular diseases. We recently showed that TMEM16A is involved in hypertension-induced cerebrovascular remodeling. However, it is unclear whether this effect is related to the...

Cite
Zheng H, Li X, Zeng X, et al. TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner. Acta Pharm Sin B. 2021;11(12):3994-4007doi: 10.1016/j.apsb.2021.04.013.
Zheng, H., Li, X., Zeng, X., Huang, C., Ma, M., Lv, X., Zhang, Y., Sun, L., Wang, G., Du, Y., & Guan, Y. (2021). TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner. Acta pharmaceutica Sinica. B, 11(12), 3994-4007. https://doi.org/10.1016/j.apsb.2021.04.013
Zheng, Huaqing, et al. "TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner." Acta pharmaceutica Sinica. B vol. 11,12 (2021): 3994-4007. doi: https://doi.org/10.1016/j.apsb.2021.04.013
Zheng H, Li X, Zeng X, Huang C, Ma M, Lv X, Zhang Y, Sun L, Wang G, Du Y, Guan Y. TMEM16A inhibits angiotensin II-induced basilar artery smooth muscle cell migration in a WNK1-dependent manner. Acta Pharm Sin B. 2021 Dec;11(12):3994-4007. doi: 10.1016/j.apsb.2021.04.013. Epub 2021 Apr 22. PMID: 35024321; PMCID: PMC8727780.
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Calcium Sensitization Mechanisms in Gastrointestinal Smooth Muscles.

Journal of neurogastroenterology and motility

Perrino BA.
PMID: 26701920
J Neurogastroenterol Motil. 2016 Apr 30;22(2):213-25. doi: 10.5056/jnm15186.

An increase in intracellular Ca(2+) is the primary trigger of contraction of gastrointestinal (GI) smooth muscles. However, increasing the Ca(2+) sensitivity of the myofilaments by elevating myosin light chain phosphorylation also plays an essential role. Inhibiting myosin light chain...

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Perrino BA. Calcium Sensitization Mechanisms in Gastrointestinal Smooth Muscles. J Neurogastroenterol Motil. 2016;22(2):213-25doi: 10.5056/jnm15186.
Perrino, B. A. (2016). Calcium Sensitization Mechanisms in Gastrointestinal Smooth Muscles. Journal of neurogastroenterology and motility, 22(2), 213-25. https://doi.org/10.5056/jnm15186
Perrino, Brian A. "Calcium Sensitization Mechanisms in Gastrointestinal Smooth Muscles." Journal of neurogastroenterology and motility vol. 22,2 (2016): 213-25. doi: https://doi.org/10.5056/jnm15186
Perrino BA. Calcium Sensitization Mechanisms in Gastrointestinal Smooth Muscles. J Neurogastroenterol Motil. 2016 Apr 30;22(2):213-25. doi: 10.5056/jnm15186. PMID: 26701920; PMCID: PMC4819859.
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