The response of mammary epithelial cells to basement membrane and stroma induced signals contributes to the degree of differentiation in this tissue. The studies reported here indicate that connective tissue growth factor (CTGF) is highly elevated during lactogenic differentiation of the HC11 mouse mammary epithelial cell line. In addition, CTGF is expressed in the mouse mammary gland during pregnancy and lactation and it is expressed in primary mammary epithelial cell cultures established from pregnant mice. In HC11 cells CTGF is transcriptionally regulated by dexamethasone, but not by estrogen or progesterone, and CTGF expression is not dependent on TGFbeta. CTGF contributes to and is required for lactogenic differentiation of HC11 cells, as demonstrated by increased differentiation following expression of plasmid-encoded CTGF and decreased differentiation following depletion of endogenous CTGF with siRNA. Moreover, HC11 mouse mammary epithelial cells infected with an adenoviral vector encoding CTGF exhibit increased lactogenic differentiation. Plasmid vector-induced elevation of CTGF levels also increased the level of beta1 integrin in HC11 cells. Because the production of stromal factors is an important component of differentiation in mammary epithelial cells, the regulation of CTGF by glucocorticoids may play a critical role in this aspect of the control of differentiation. The studies reported here provide important information on the role of CTGF in mammary epithelial cell differentiation.

The role of lipoxygenase and cyclooxygenase metabolites in acute hypoxic pulmonary vasoconstriction (HPV) was studied in piglets. It has been found that acute alveolar hypoxia induced remarkable pulmonary vasoconstriction, associated with an increase in cardiac output. The hypoxic pulmonary vasoconstriction response was insignificantly attenuated after infusion of DEC. Indomethacin potentiated markedly the increase in pulmonary artery pressure and pulmonary vascular resistance and thus augmented HPV. It is inferred that hypoxic pulmonary vasoconstriction in piglet may be mediated by other important mediators in addition to leukotrienes, but modulated by prostaglandins to prevent an excessive rise in pulmonary artery pressure.

The aim of this study was to investigate the role of sympathetic nerve and adrenal gland in the changes in hemodynamics and hypoxic pulmonary vasoconstriction (HPV) induced by cigarette smoking in Wistar rats. Data showed that an increment of pulmonary vascular resistance (PVR) induced by alveolar hypoxia was partially prevented by prazosin (alpha 1-receptor blocker) and prazosin combined with propranolol (beta-receptor blocker), but not significantly affected by propranolol or adrenalectomy. Cigarette smoking could increase PVR and potentiate HPV, whereas the potentiation of HPV was partially inhibited by prazosin and strengthened by propranolol, but not affected by adrenalectomy. It is suggested that the sympathetic nerve excitation caused by cigarette smoking may play a role in the strengthening of HPV.