Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 287, Issue 6, Pages L1107-L1115Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00119.2004
Keywords
dog; postnatal development and maturation; compensatory lung growth; apoptosis; immunohistochemistry; immunoblot
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Funding
- NHLBI NIH HHS [HL-62873, HL-54060, R01-HL-40070, HL-45716, R01 HL040070, R01 HL062873, R01 HL045716, R01 HL054060] Funding Source: Medline
- NIDDK NIH HHS [R01-DK-48482, DK-64396] Funding Source: Medline
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Circulating erythropoietin (EPO) stimulates erythrocytosis, whereas organ-specific local EPO receptor ( EPOR) expression has been linked to angiogenesis, tissue growth, and development. On the basis of the observation of concurrent enhancement of lung growth and erythrocyte production during exposure to chronic hypoxia, we hypothesized that a paracrine EPO system is involved in mediating lung growth. We analyzed EPOR protein expression in normal dog lung tissue during postnatal maturation and during compensatory lung growth after right pneumonectomy (PNX). Membrane-bound EPOR was significantly more abundant in the immature lung compared with mature lung and in the remaining lung 3 wk after PNX compared with matched sham controls. COOH-terminal cytosolic EPOR peptides, which were even more abundant than membrane-bound EPOR, were also upregulated in immature lung but differentially processed after PNX. Apoptosis was enhanced during both types of lung growth in direct relationship to cellular proliferation and EPOR expression. We conclude that both developmental and compensatory lung growth involve paracrine EPO signaling with parallel upregulation but differential processing of EPOR.
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