Developmental regulation of p66Shc is altered by bronchopulmonary dysplasia in baboons and humans.

ABSTRACT:

Rationale

The p66(Shc) adapter protein antagonizes mitogen-activated protein, or MAP, kinase, mediates oxidative stress, and is developmentally regulated in fetal mouse lungs.

Objectives

To determine if p66(Shc) is similarly regulated in primates and in bronchopulmonary dysplasia (BPD), which results from oxidative injury to immature lungs.

Methods

Normal and injured lungs from humans and baboons were evaluated by Western analysis and immunohistochemistry.

Measurements and main results

In baboons, p66(Shc) decreased 80% between 125 and 175 days' gestation (p = 0.025), then doubled after term delivery at 185 days (p = 0.0013). In the hyperoxic 140-day fetal baboon BPD model, p66(Shc) expression persisted, and its localization shifted from the epithelium of gesta

SUBMITTER: Lee MK 

PROVIDER: S-EPMC2718481 | biostudies-literature | 2005 Jun

REPOSITORIES: biostudies-literature