The goal of the present proposal is increase the community of academic researchers motivated and capable of carrying out hypothesis-driven research to address questions in pulmonary diseases, and to specifically create a new research focus within our Center, concentrated on the biology of the developing lung. The goal will be achieved by the recruitment and support of a newly independent investigator, Dr. Cristina Alvira, in the manner outlined by this proposal. The recruitment of Dr. Alvira will allow for the development of a Core Center within the Center for Excellence in Pulmonary Biology at Stanford University to conduct multidisciplinary, biomedical research to elucidate the molecular mechanisms that direct alveolar development. This Core Center will emphasize three fundamental scientific goals: (i) identification of the signaling pathways that allow for the transition between the sacular and alveolar stages of lung development;(ii) exploration of the interplay between postnatal vascular and alveolar development;and (iii) determination of the long-term implications of early disruption of alveolarization on future lung growth and function. Recent evidence already supports the notion that injury during this critical window of lung development may represent the childhood antecedent of adult disease, with such insults falling upon susceptible hosts, and resulting in the development of pulmonary diseases such idiopathic pulmonary fibrosis, pulmonary hypertension, interstitial lung disease, asthma or emphysema. Therefore, identification of factors that either promote or disrupt alveolar development might be readily translated into the development of novel therapeutics with potential applicability to numerous forms of lung disease affecting both children and adults. A panel of senior faculty, representing a plethora of scientific disciplines, will serve to enhance the depth and scope of her emerging research program, and further increase the likelihood of her continued academic success. Furthermore, extensive resources from the Center for Excellence in Pulmonary Biology, the Department of Pediatrics, and Stanford University School of Medicine as a whole will be readily available to Dr. Alvira as a testament to the Institutional support for this deserving candidate.

Public Health Relevance

The present application seeks funds that will optimize the likelihood of success for a compelling, wellqualified woman of Hispanic descent to succeed in the arena of basic research focused upon the biology of the developing lung, allowing Dr. Cristina M. Alvira to contribute significant new knowledge to the pulmonary biology community and serve as a role model for the next generation of young physician scientists.

National Institute of Health (NIH)
National Heart, Lung, and Blood Institute (NHLBI)
Center Core Grants (P30)
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Special Emphasis Panel (ZHL1-CSR-E (O1))
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Rothgeb, Ann E
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Stanford University
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Hou, Yanli; Liu, Min; Husted, Cristiana et al. (2015) Activation of the nuclear factor-?B pathway during postnatal lung inflammation preserves alveolarization by suppressing macrophage inflammatory protein-2. Am J Physiol Lung Cell Mol Physiol 309:L593-604
Baker, Christopher D; Alvira, Cristina M (2014) Disrupted lung development and bronchopulmonary dysplasia: opportunities for lung repair and regeneration. Curr Opin Pediatr 26:306-14
Ahn, Yong-Tae; Kim, Yu-Mee; Adams, Eloa et al. (2012) Hypoxia-inducible factor-1ýý regulates KCNMB1 expression in human pulmonary artery smooth muscle cells. Am J Physiol Lung Cell Mol Physiol 302:L352-9
Merk, Denis R; Chin, Jocelyn T; Dake, Benjamin A et al. (2012) miR-29b participates in early aneurysm development in Marfan syndrome. Circ Res 110:312-24
Iosef, Cristiana; Alastalo, Tero-Pekka; Hou, Yanli et al. (2012) Inhibiting NF-?B in the developing lung disrupts angiogenesis and alveolarization. Am J Physiol Lung Cell Mol Physiol 302:L1023-36
Alvira, Cristina M; Umesh, Anita; Husted, Cristiana et al. (2012) Voltage-dependent anion channel-2 interaction with nitric oxide synthase enhances pulmonary artery endothelial cell nitric oxide production. Am J Respir Cell Mol Biol 47:669-78