method-for-obtaining-primary-ovarian-cancer-cells-from-solid-specimens

Method for Obtaining Primary Ovarian Cancer Cells From Solid Specimens

Reliable tools for investigating ovarian cancer initiation and progression are urgently needed. While the use of ovarian cancer cell lines remains a ...

Maricopa Medical Center and St Josephs Hospital and Medical Center

In 2009, the North West Local Health Integration Network hosted Share Your Story, Shape Your Care, an innovative community engagement initiative. Over 800 residents and health service providers in Northwestern Ontario participated and identified healthcare priorities, reacted to proposed strategies and shared ideas and stories. Primarily web-based (with a Choicebook, message board, blog and YouTube video), paper copies and conversation guides supported informed and reflective participation. This project enabled community-level participation in healthcare, supporting local planning and decision-making, and was awarded the inaugural Innovation Using Technology Award by the International Association for Public Participation.

Share your story, shape your care: engaging the diverse and disperse population of Northwestern Ontario in healthcare priority setting.

Although mitogen-activated protein kinase phosphatase-1 (MKP-1) is a key deactivator of MAP kinases, known effectors of lung vessel formation, whether it plays a role in the expression of proangiogenic vascular endothelial growth factor (VEGF) in hypoxic lung is unknown. We therefore hypothesized that MKP-1 is a crucial modulator of hypoxia-stimulated vessel development by regulating lung VEGF levels. Wild-type MKP-1(+/+), heterozygous MKP-1(+/-), and deficient MKP-1(-/-) mice were exposed to sea level (SL), Denver altitude (DA) (1609 m [5280 feet]), and severe high altitude (HYP) (∼5182 m [∼17,000 feet]) for 6 weeks. Hypoxia enhanced phosphorylation of p38 MAP kinase, a substrate of MKP-1, as well as α smooth muscle actin (αSMA) expression in vessels, respiratory epithelium, and interstitium of phosphatase-deficient lung. αSMA-positive vessel (<50 μm outside diameter) densities were markedly reduced, whereas vessel wall thickness was increased in hypoxic MKP-1(-/-) lung. Mouse embryonic fibroblasts (MEFs) of all three genotypes were isolated to pinpoint the mechanism involved in hypoxia-induced vascular abnormalities of MKP-1(-/-) lung. Sustained phosphorylation of p38 MAP kinase was observed in MKP-1-null MEFs in response to hypoxia exposure. Although hypoxia up-regulated VEGF levels in MKP-1(+/+) MEFs eightfold, only a 70% increase in VEGF expression was observed in MKP-1-deficient cells. Therefore, our data strongly suggest that MKP-1 might be the key regulator of vascular densities through the regulation of VEGF levels in hypoxic lung.

Mitogen-activated protein kinase phosphatase-1 is a key regulator of hypoxia-induced vascular endothelial growth factor expression and vessel density in lung.

Article	Year
Share your story, shape your care: engaging the diverse and disperse population of Northwestern Ontario in healthcare priority setting. Healthcare quarterly (Toronto, Ont.)\| PubMed ID: 20523159	2010
Mitogen-activated protein kinase phosphatase-1 is a key regulator of hypoxia-induced vascular endothelial growth factor expression and vessel density in lung. The American journal of pathology\| PubMed ID: 21224048	2011

Kristin Shields

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