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Published ahead of print on June 5, 2003, doi:10.1165/rcmb.2002-0314OC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 6, December 2003, 733-742

A more recent version of this article appeared on December 1, 2003
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Submitted on December 27, 2002
Revised on June 3, 2003

Pro-apoptotic effects of parathyroid hormone-related protein in type II pneumocytes

Randolph H Hastings1*, Rick A Quintana2, Rebeca Sandoval2, Devin Duey2, Yvette Rascon2, Douglas W Burton3, and Leonard J Deftos3

1 Research, VA San Diego Healthcare System, San Diego, CA, USA; Anesthesiology, VA San Diego Healthcare System, San Diego, CA, USA; Anesthesiology, University of California, San Diego, San Diego, CA, USA, 2 Research, VA San Diego Healthcare System, San Diego, CA, USA, 3 Research, VA San Diego Healthcare System, San Diego, CA, USA; Medicine, VA San Diego Healthcare System, San Diego, CA, USA; Medicine, University of California, San Diego, San Diego, CA, USA

* To whom correspondence should be addressed. E-mail: rhhastings{at}ucsd.edu.

Parathyroid hormone-related protein (PTHrP) promotes or suppresses apoptosis in various settings depending on cell type and context. PTHrP 1-34 and PTHrP 67-86 are type II cell growth factors with effects on pneumocyte growth and surfactant secretion. This study investigated the effects of 24 h pretreatment with these two peptides on rat type II cell apoptosis after 0.3 J/cm2 UV-B irradiation. Adherent cells decreased in number by 15 ± 5% and nonadherent cells increased over five-fold 24 h after UV. Cell loss was due predominantly to apoptosis, based on ethidium bromide exclusion, nuclear condensation, and caspase 3 activity. Nuclear condensation increased from 15.6 ± 2.2% of irradiated cells with no treatment to 25.6 ± 4.9 and 22.9 ± 1.8% of cells in UV/PTHrP 1-34 and UV/PTHrP 67-86 groups, respectively (P <0.01), along with a 60% increase in caspase 3 activity. Effects on apoptosis were unaffected by the presence or absence of serum, but were ameliorated by growth to confluency or adherence to fibronectin. PTHrP 1-34 and PTHrP 67-86 augmented inositol phosphate levels, but had minimal effects on cAMP. Thus, PTHrP 1-34 and PTHrP 67-86 sensitize type II cells to apoptosis, possibly by a phospholipase C-dependent mechanism. The effects appear to be regulated by cell-matrix and cell-cell interactions.




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