Identification of an up-regulated anti-apoptotic network in the internal thoracic artery

Krane, Markus; Dummler, Sara; Dreßen, Martina; Hauner, Hans; Hoffmann, Micha; Haller, Dirk; Heller, Katharina; Wildhirt, Stephen M.; Voß, Bernhard; Grammer, Joachim B.; Lahm, Harald; Lange, Rüdiger; Bauernschmitt, Robert

doi:10.1016/j.ijcard.2010.02.003

Cited by 2 publications

(2 citation statements)

References 38 publications

(40 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The total area was nearly 3,300,000 µm 2 in each group. After microdissection, tissues were pooled together for total RNA extraction using an RNeasy FFPE Kit (Qiagen, Hilden, Germany) [13,14]. Synthesis of cDNA from total RNA was carried out using High Capacity RNA-to-cDNA Master Mix (Applied Biosystems, Foster City, Calif., USA).…”

Section: Methodsmentioning

confidence: 99%

Renin Angiotensin Antagonists Normalize Aberrant Activation of Epithelial Sodium Channels in Sodium-Sensitive Hypertension

Ushio-Yamana

Minegishi

Ishigami

et al. 2013

Nephron Exp Nephrol

View full text Add to dashboard Cite

Epithelial sodium channels (ENaC) are ion transporters in the aldosterone-sensitive distal nephron that play an important role in sodium reabsorption in the terminal nephron. Our study of inbred C57Bl6/J mice given a high-sodium diet showed increased ENaC expression accompanied by tubular renin activation on qRT-PCR of laser-captured tubule specimens and Western blotting of membrane proteins, despite inhibition of aldosterone. Treatment with an angiotensin-converting-enzyme inhibitor (ACEI) or an angiotensin receptor blocker (ARB) effectively lowered blood pressure. In addition to lowering blood pressure, ACEI and ARB inhibition downregulated ENaC and renin expression in renal tubules. These effects would act to suppress sodium reabsorption via ENaC and normalize molecular mechanisms that elevate blood pressure in response to increased salt intake.

show abstract

Section: Methodsmentioning

confidence: 99%

Renin Angiotensin Antagonists Normalize Aberrant Activation of Epithelial Sodium Channels in Sodium-Sensitive Hypertension

Ushio-Yamana

Minegishi

Ishigami

et al. 2013

Nephron Exp Nephrol

View full text Add to dashboard Cite

show abstract

“…One such factor is mechanotransduction, the cellular event whereby mechanical stimuli are converted into biochemical signals. In vivo , cells may experience mechanical forces through the pulsatile nature of blood flow or during the process of wound contraction [18], [19]. Fibroblasts play a key role in granulation tissue formation during the proliferative phase of wound healing.…”

Section: Introductionmentioning

confidence: 99%

The Effect of p38MAPK on Cyclic Stretch in Human Facial Hypertrophic Scar Fibroblast Differentiation

Zhang

Chen

et al. 2013

PLoS ONE

View full text Add to dashboard Cite

Hypertrophic scars (HTS), the excessive deposition of scar tissue by fibroblasts, is one of the most common skin disorders. Fibroblasts derived from surgical scar tissue produce high levels of α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1). However, the molecular mechanisms for this phenomenon is poorly understood. Thus, the purpose of this study was to evaluate the molecular mechanisms of HTS and their potential therapeutic implications. Fibroblasts derived from skin HTS were cultured and characterized in vitro. The fibroblasts were synchronized and randomly assigned to two groups: cyclic stretch and cyclic stretch pre-treated with SB203580 (a p38MAPK inhibitor). Cyclic stretch at 10% strain was applied at a loading frequency of 10 cycles per minute (i.e. 5 seconds of tension and 5 seconds of relaxation) for 0 h, 6 h and 12 h. Cyclic stretch on HTS fibroblasts led to an increase in the expression of α-SMA and TGF-β1 mRNA and protein and the phosphorylation of p38MAPK. SB203580 reversed these effects and caused a decrease in matrix contraction. Furthermore, HTS fibroblast growth was partially blocked by p38MAPK inhibition. Therefore, the mechanism of cyclic stretch involves p38 MAPK, and its inhibition is suggested as a novel therapeutic strategy for HTS.

show abstract

Identification of an up-regulated anti-apoptotic network in the internal thoracic artery

Cited by 2 publications

References 38 publications

Renin Angiotensin Antagonists Normalize Aberrant Activation of Epithelial Sodium Channels in Sodium-Sensitive Hypertension

Renin Angiotensin Antagonists Normalize Aberrant Activation of Epithelial Sodium Channels in Sodium-Sensitive Hypertension

The Effect of p38MAPK on Cyclic Stretch in Human Facial Hypertrophic Scar Fibroblast Differentiation

Contact Info

Product

Resources

About