Extra cellular matrix biology and myocardial remodeling

Factors associated with posttraumatic growth among the spouses of myocardial infarction patients

by Mithat Durak

Key Words: cognitive processing, environmental factors, individual factors, myocardial infarction patients, posttraumatic growth, spouses of myocardial infarction patients

To clarify the rationale behind Posttraumatic Growth (PTG), a model by Schaefer and Moos describes the relative... more To clarify the rationale behind Posttraumatic Growth (PTG), a model by Schaefer and Moos describes the relative contribution of environmental resources, individual resources, event related factors, cognitive processing and coping (CPC) on PTG. In the present study, this model was tested with the spouses of myocardial infarction patients with data from various hospitals in Turkey. A structural equation model revealed that neither individual nor environmental resources had indirect effects on PTG through the effect of event-related factors and CPC, while they showed direct effects on PTG. The findings were discussed in the context of the theoretical model.

Factors Associated with Posttraumatic Growth Among Myocardial Infarction Patients: Perceived Social Support, Perception of the Event and Coping

by Mithat Durak

Key Words: Posttraumatic growth, Perceived social support, Perception of the event, Coping, Myocardial infarction patients

Posttraumatic Growth (PTG) is accepted as positive transformations that are a product of struggling with significant... more Posttraumatic Growth (PTG) is accepted as positive transformations that are a product of struggling with significant stressors such as chronic illness. A model, conceptualized by Schaefer and Moos (Posttraumatic growth: Positive changes in the aftermath of crisis, pp 99–126, 1998), suggests a relative contribution of environmental and individual resources, perception of the event (PE) and coping in the development of PTG. The aim of the present study was to examine the effect of perceived social support (PSS), PE and coping on PTG. This model was tested in a sample of patients with myocardial infarction (MIP, N = 148) from various hospitals in Turkey. The structural equation analysis of the model revealed that PSS was significantly related to PTG through the effect of coping. While coping was significantly and directly related to PTG, PE was not. The findings are discussed in the context of the theoretical model with suggestions for future research.

REGULATION OF ENDOTHELIAL NITRIC OXIDE SYNTHASE LOCALIZATION IN PULMONARY MYOFIBROBLASTS

by Jon Faughn

Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease leading to decreased lung volume and eventual... more Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease leading to decreased lung volume and eventual respiratory failure. At present, the median post-diagnosis lifespan is between three and six years. Myofibroblasts are collagen-secreting cells essential for wound healing, but also implicated in the fibroproliferation and extra cellular matrix deposition commonly seen in IPF. The nitric oxide (NO) signaling pathway is implicated in protomyofibroblast to myofibroblast transition and regulation. Previous work has shown that in pulmonary myofibroblasts, endothelial nitric oxide synthase (eNOS) is the primary NOS isoform expressed. The current study used cultured rat pulmonary myofibroblasts between passages two and five as a cell model. The cells were grown in normal growth media (DMEM + 10% FBS) or serum starved (DMEM + 0% FBS) to induce cellular differentiation. In this study, immunocytochemistry was used to show localization of eNOS is dependent on cellular differentiation, with protomyofibroblasts expressing eNOS primarily in the nucleus and protomyofibroblasts expressing eNOS in the perinuclear region. We also show catalytic activity and localization of eNOS are correlated by visualizing nitric oxide production in the cells using a permeable fluorescein chromophore. By using western blot analysis on fractionated cell lysates we found eNOS expressed in the nucleus under normal growth conditions. eNOS is at least partially regulated by intracellular calcium (Ca2+) and calmodulin (CaM). Western blot analysis using native eNOS and phospho-specific eNOS antibodies on fractionated cells treated with the protein kinase C (PKC) activator phorbal 12-myristate 13-acetate (PMA) with and without addition of its antagonist ethylene glycol tetraacetic acid (EGTA) was conducted to investigate PKC’s role in eNOS regulation by phosphorylation. Indeed, PKC activation was found to mitigate expression in the nucleus, while inhibition of the activator restored the activity expression above basal levels. This finding correlates with previous data from our lab showing a decrease in activity in myofibroblasts treated with PMA and assayed amperometrically with an NO electrode.