Determination of PKC isoform-specific protein expression in pulmonary arteries of rats with chronic hypoxia-induced pulmonary hypertension

Shi, Yiwei; Wang, Chen; Han, Song; Pang, Bao-sen; Zhang, Nan; Wang, Jun; Li, Junfa

doi:10.12659/msm.882458

Cited by 13 publications

(5 citation statements)

References 38 publications

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“…The authors suggest that the attack of reactive oxygen species during the oxidative stress primarily affects the saturation level of fatty acyl chains and the phospholipid structure. 7,8 In contrast to systemic hypertension that is diagnosed on the basis of simple systemic blood pressure measurements, the diagnosis of PAH requires a combination of tests, e.g. This approach included a method of identification and quantification of several serum protein parameters from one ATR FTIR spectrum such as the content of total albumin, globulin and immunoglobulin as well as their relative contribution to the overall protein composition.…”

Section: Introductionmentioning

confidence: 99%

“…PAH is a chronic progressive disease of the pulmonary vasculature, characterized by an elevated pulmonary arterial pressure leading to right ventricular failure. 7,8 In contrast to systemic hypertension that is diagnosed on the basis of simple systemic blood pressure measurements, the diagnosis of PAH requires a combination of tests, e.g. functional assessment, exercise tolerance, laboratory tests, magnetic resonance imaging, and echocardiography to support right heart hypertrophy or failure.…”

Section: Introductionmentioning

confidence: 99%

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Plasma biomarkers of pulmonary hypertension identified by Fourier transform infrared spectroscopy and principal component analysis

Staniszewska-Slezak

Fedorowicz

Kramkowski

et al. 2015

Analyst

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The main goal of this study was to find specific plasma spectral markers associated with pulmonary arterial hypertension (PAH) induced by monocrotaline injection in rats. FTIR was used to monitor biochemical changes in plasma caused by PAH as compared with the systemic hypertension induced by partial ligation on the left artery and with the control group. Both pathologies, systemic and pulmonary hypertension, induced a unique response in the biochemical content of plasma, mainly related to the composition and secondary structure of plasma proteins. For PAH, β-pleated sheet components of plasma proteins were identified whereas the protein composition in systemic hypertension was dominated by unordered structures. In addition, a higher concentration of tyrosine-rich proteins was found in plasma in PAH than in systemic hypertension. The differences between both pathologies were identified also in terms of lipid composition/metabolism as well as in the content of RNA and glucose, suggesting that lipid peroxidation appears upon pulmonary hypertension development. In summary, this work demonstrates that FTIR spectroscopy supported by principal component analysis (PCA) has the potential to become a fast and non-destructive method for biochemical characterization of plasma that consequently could have a diagnostic significance in pulmonary hypertension.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Plasma biomarkers of pulmonary hypertension identified by Fourier transform infrared spectroscopy and principal component analysis

Staniszewska-Slezak

Fedorowicz

Kramkowski

et al. 2015

Analyst

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“…Previous studies have reported that androgens play a critical role in cardiovascular disease [ 20 ] and are associated with pulmonary arterial hypertension [ 21 ], and AR had been identified in the right and left ventricles [ 22 ]. The changes in membrane translocation and protein expression of cPKC α , β I, β II, and nPKC δ are involved in the development of hypoxia-induced rat pulmonary hypertension [ 23 ]. An organized thrombus in major pulmonary arteries is typically in association with other diseases, such as lung cancer [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Microarray Analysis and Detection of MicroRNAs Associated with Chronic Thromboembolic Pulmonary Hypertension

Miao

Wang

Wan

et al. 2017

BioMed Research International

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The aim of this study was to understand the importance of chronic thromboembolic pulmonary hypertension- (CTEPH-) associated microRNAs (miRNAs). miRNAs differentially expressed in CTEPH samples compared with control samples were identified, and the target genes were predicted. The target genes of the key differentially expressed miRNAs were analyzed, and functional enrichment analyses were carried out. Finally, the miRNAs were detected using RT-PCR. Among the downregulated miRNAs, MiR-3148 regulated the most target genes and was significantly enriched in pathways in cancer, glioma, and ErbB signaling pathway. Furthermore, the number of target genes coregulated by miR-3148 and other miRNAs was the most. AR (androgen receptor), a target gene of hsa-miR-3148, was enriched in pathways in cancer. PRKCA (Protein Kinase C Alpha), also a target gene of hsa-miR-3148, was enriched in 15 of 16 KEGG pathways, such as pathways in cancer, glioma, and ErbB signaling pathway. In addition, the RT-PCR results showed that the expression of hsa-miR-3148 in CTEPH samples was significantly lower than that in control samples (P < 0.01). MiR-3148 may play an important role in the development of CTEPH. The key mechanisms for this miRNA may be hsa-miR-3148-AR-pathways in cancer or hsa-miR-3148-PRKCA-pathways in cancer/glioma/ErbB signaling pathway.

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“…A study by Shi et al [46 ]demonstrated decreased PKCα expression in the pulmonary arteries of rats with hypoxia-induced pulmonary hypertension. Moreover, increased TP receptor density has been observed in the right ventricular tissue of PAH patients [47].…”

Section: Discussionmentioning

confidence: 99%

PKCα Deficiency in Mice Is Associated with Pulmonary Vascular Hyperresponsiveness to Thromboxane A2 and Increased Thromboxane Receptor Expression

Tabeling

Noe²,

Naujoks³

et al. 2015

J Vasc Res

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Pulmonary vascular hyperresponsiveness is a main characteristic of pulmonary arterial hypertension (PAH). In PAH patients, elevated levels of the vasoconstrictors thromboxane A2 (TXA2), endothelin (ET)-1 and serotonin further contribute to pulmonary hypertension. Protein kinase C (PKC) isozyme alpha (PKCα) is a known modulator of smooth muscle cell contraction. However, the effects of PKCα deficiency on pulmonary vasoconstriction have not yet been investigated. Thus, the role of PKCα in pulmonary vascular responsiveness to the TXA2 analog U46619, ET-1, serotonin and acute hypoxia was investigated in isolated lungs of PKCα^-/- mice and corresponding wild-type mice, with or without prior administration of the PKC inhibitor bisindolylmaleimide I or Gö6976. mRNA was quantified from microdissected intrapulmonary arteries. We found that broad-spectrum PKC inhibition reduced pulmonary vascular responsiveness to ET-1 and acute hypoxia and, by trend, to U46619. Analogously, selective inhibition of conventional PKC isozymes or PKCα deficiency reduced ET-1-evoked pulmonary vasoconstriction. The pulmonary vasopressor response to serotonin was unaffected by either broad PKC inhibition or PKCα deficiency. Surprisingly, PKCα^-/- mice showed pulmonary vascular hyperresponsiveness to U46619 and increased TXA2 receptor (TP receptor) expression in the intrapulmonary arteries. To conclude, PKCα regulates ET-1-induced pulmonary vasoconstriction. However, PKCα deficiency leads to pulmonary vascular hyperresponsiveness to TXA2, possibly via increased pulmonary arterial TP receptor expression.

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Determination of PKC isoform-specific protein expression in pulmonary arteries of rats with chronic hypoxia-induced pulmonary hypertension

Cited by 13 publications

References 38 publications

Plasma biomarkers of pulmonary hypertension identified by Fourier transform infrared spectroscopy and principal component analysis

Plasma biomarkers of pulmonary hypertension identified by Fourier transform infrared spectroscopy and principal component analysis

Microarray Analysis and Detection of MicroRNAs Associated with Chronic Thromboembolic Pulmonary Hypertension

PKCα Deficiency in Mice Is Associated with Pulmonary Vascular Hyperresponsiveness to Thromboxane A2 and Increased Thromboxane Receptor Expression

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