Vasoactive intestinal peptide gene alterations in patients with idiopathic pulmonary arterial hypertension.

Pulmonary arterial hypertension is a progressive disease, characterised by increased proliferation of pulmonary artery smooth muscle cells, vasoconstriction and remodelling of the vascular wall leading to right heart failure and death. The idiopathic form is rare (idiopathic arterial primary hypertension (IPAH); formerly PPH, MIM# 178600). Our group correlated a deficiency in vasoactive intestinal peptide (VIP; MIM# 192320) levels in serum and lung tissue with the pathogenesis of IPAH.

The vasoactive intestinal peptide receptor turnover in pulmonary arteries indicates an important role for VIP in the rat lung circulation.

Vasoactive intestinal peptide (VIP) is a potent vasorelaxing peptide that plays a role in lung physiology and possibly in pulmonary hypertension. We investigated the turnover of the VIP receptors on rat pulmonary arteries ex vivo. There was evidence for a fast receptor turnover in pulmonary arteries, which underlines the important role of VIP for the regulation of pulmonary circulation and pulmonary pathology.

New nonradioactive technique for vasoactive intestinal peptide-receptor-ligand-binding studies.

We describe fluorescent-labeled peptide (FLP) studies on living cells. The new technique is nonradioactive and it allows monitoring of the binding and internalization of Vasoactive Intestinal Peptide (VIP) in VIP receptor-expressing cells. The technique is easy to perform and the observed reaction is peptide sequence specific.

Palisade endings in extraocular muscles of the monkey are immunoreactive for choline acetyltransferase and vesicular acetylcholine transporter.

Purpose: To analyze palisade endings in extraocular muscles (EOMs) of a primate species and to examine our previous findings in cat that palisade endings are putative effector organs.

Methods: Eleven monkeys (Macaca fascicularis) of both sexes, between 4 and 6 years of age were analyzed. Whole EOM myotendons were immunostained with four combinations of triple-fluorescent labeling and examined by confocal laser scanning microscopy.

The differentiation inducers phenylacetate and phenylbutyrate modulate camptothecin sensitivity in colon carcinoma cells in vitro by intracellular acidification.

Aromatic fatty acids such as phenylbutyrate (PB) and its metabolite phenylacetate (PA) induce growth arrest, differentiation and apoptosis in solid tumor cells. Despite their antiproliferative action they were reported to exhibit a synergistic effect in combination with cytotoxic drugs like topotecan, and others. Since the activity of the camptothecines (CPTs) depends on local pH conditions, we investigated, whether PB/PA modulate CPT effects indirectly by affecting intracellular pH in SW620 and SW480 colon cancer cells.