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Data for increased Rho kinase activity in type 2 diabetic patients.

ABSTRACT: 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. These data describe the observed relationship of Rho-Kinase activity with type 2 diabetic patients. Rho-Kinase activity is determined by immunoblotting of peripheral blood leukocytes with the Phospho-Thr853 in the myosin-binding subunit of myosin light-chain phosphatase. The level of IL-6 is measured using Enzyme-linked immunosorbent assay.

SUBMITTER: Liu L

PROVIDER: S-EPMC5120266 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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Data for increased Rho kinase activity in type 2 diabetic patients.

Liu Lei L Tan Lun L Lai Jinsheng J Li Sheng S Wang Dao Wen DW

Data in brief 20161116

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. These data describe the observed relationship of Rho-Kinase activity with type 2 diabetic patients. Rho-Kinase activity is determined by immunoblotting of peripheral blood leukocytes with the Phospho-Thr853 in the myosin-bindin ...[more]

PMID: 27896306

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Project description:Formaldehyde, a common indoor air pollutant, exacerbates asthma and synergizes with allergen to induce airway hyperresponsiveness (AHR) in animal models. The mechanisms mediating formaldehyde-induced AHR remain poorly understood. We posit that formaldehyde modulates agonist-induced contractile response of human airway smooth muscle (HASM) cells to elicit AHR. HASM cells were exposed to formaldehyde or vehicle and agonist-induced intracellular Ca2+ ([Ca2+]i) and myosin light-chain phosphatase (MYPT1) phosphorylation were determined. Air-liquid interface-differentiated human bronchial epithelial (HBE) cells were exposed to formaldehyde or vehicle and cocultured with HASM cells. Agonist-induced [Ca2+]i and MYPT1 phosphorylation were determined in the cocultured HASM cells. Precision-cut human lung slices were exposed to PBS or varying concentrations of formaldehyde, and then carbachol-induced airway narrowing was determined 24 hours after exposure. HASM cells were transfected with nontargeting or nuclear factor erythroid-derived 2, like 2 (Nrf-2)-targeting small interfering RNA and exposed to formaldehyde or vehicle, followed by determination of antioxidant response (quinone oxido-reductase 1 and thioredoxin 1) and basal and agonist-induced MYPT1 phosphorylation. Formaldehyde enhanced the basal Rho-kinase activity and MYPT1 phosphorylation with little effect on agonist-induced [Ca2+]i in HASM cells. Formaldehyde induced Nrf-2-dependent antioxidant response in HASM cells, although the MYPT1 phosphorylation was independent of Nrf-2 induction. Although HBE cells exposed to formaldehyde had little effect on agonist-induced [Ca2+]i or MYPT1 phosphorylation in cocultured HASM cells, formaldehyde enhanced carbachol-induced airway responsiveness in precision-cut human lung slices. In conclusion, formaldehyde induces phosphorylation of the regulatory subunit of MYPT1, independent of formaldehyde-induced Nrf-2 activation in HASM cells. The findings suggest that the Rho kinase-dependent Ca2+ sensitization pathway plays a role in formaldehyde-induced AHR.

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Data for increased Rho kinase activity in type 2 diabetic patients.

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Data for increased Rho kinase activity in type 2 diabetic patients.

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