A novel method for detection of apoptosis.

There are two different Angiotensin II (ANG II) peptides in nature: Human type (ANG II) and Bovine type (ANG II). These eight amino acid peptides differ only at position 5 where Valine is replaced by Isoleucine in the Bovine type. They are present in all species studied so far.

Role of meconium and hypoxia in meconium aspiration-induced lung injury in neonatal rabbits.

Background: We previously showed that meconium causes lung cell death by apoptosis and inflammatory cytokine expression. Whether this is due to meconium exposure itself, or meconium related hypoxia remains unclear.

Objectives: To elucidate the effects of meconium, saline, milk, hypoxia and hyperoxia induced lung injury.

Meconium-induced release of nitric oxide in rabbit alveolar cells.

Previous studies have shown meconium-induced lung injury occurs throughout release of inflammatory cytokines. The exact mechanism of cytokine-induced apoptosis is not known. In this study we hypothesized that meconium-induced apoptosis in the lungs is mediated through the production of inducible nitric oxide (NO).

Studies of meconium-induced lung injury: inflammatory cytokine expression and apoptosis.

To review current literature related to cellular mechanisms of meconium-induced lung injury (MILI). Review of published experimental in vitro and in vivo MAS studies using human and animal lung cells. We found that meconium induces expression of cytokines and angiotensin II (ANG II)-induced apoptotic process in the lung cells.

Meconium increases type 1 angiotensin II receptor expression and alveolar cell death.

The pulmonary renin-angiotensin system (RAS) contributes to inflammation and epithelial apoptosis in meconium aspiration. It is unclear if both angiotensin II receptors (ATR) contribute, where they are expressed and if meconium modifies subtype expression. We examined ATR subtypes in 2 wk rabbit pup lungs before and after meconium exposure and with and without captopril pretreatment or type 1 receptor (AT1R) inhibition with losartan, determining expression and cellular localization with immunoblots, RT-PCR and immunohistochemistry, respectively.