Structural, functional and molecular analysis of the effects of aging in the small intestine and colon of C57BL/6J mice.

Background: By regulating digestion and absorption of nutrients and providing a barrier against the external environment the intestine provides a crucial contribution to the maintenance of health. To what extent aging-related changes in the intestinal system contribute to the functional decline associated with aging is still under debate.

Methods: Young (4 M) and old (21 M) male C57BL/6J mice were fed a control low-fat (10E%) or a high-fat diet (45E%) for 2 weeks.

The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice.

Background: Obesity and insulin resistance are two major risk factors underlying the metabolic syndrome. The development of these metabolic disorders is frequently studied, but mainly in liver, skeletal muscle, and adipose tissue. To gain more insight in the role of the small intestine in development of obesity and insulin resistance, dietary fat-induced differential gene expression was determined along the longitudinal axis of small intestines of C57BL/6J mice.

Bradykinin augments EGF-induced airway smooth muscle proliferation by activation of conventional protein kinase C isoenzymes.

This study aims to investigate the effects of bradykinin, alone and in combination with growth factors on proliferation of cultured bovine tracheal smooth muscle cells. Bradykinin did not induce mitogenic responses by itself, but concentration-dependently augmented growth factor-induced [3H]thymidine incorporation and cell proliferation. The bradykinin effect was mediated by bradykinin B2 receptors, and not dependent on cyclo-oxygenase.

Growth factor-induced contraction of human bronchial smooth muscle is Rho-kinase-dependent.

Growth factors have been implicated in the pathophysiology of asthma. However, the putative effects of these growth factors on human airway smooth muscle tone are still largely unknown. We performed contraction experiments using human bronchial smooth muscle ring preparations.

Muscarinic M(3) receptor-dependent regulation of airway smooth muscle contractile phenotype.

1. Airway smooth muscle (ASM) cells are known to switch from a contractile to a proliferative and synthetic phenotype in culture in response to serum and growth factors. Phenotype switching in response to contractile agonists, however, is poorly characterised, despite the possible relationship between ASM phenotype and airway remodelling in asthma.

Insulin induces a hypercontractile airway smooth muscle phenotype.

This study aims to investigate the effects of insulin on bovine tracheal smooth muscle phenotype in vitro. Contractility of muscle strips and DNA-synthesis ([3H]thymidine incorporation) of isolated cells were used as parameters for smooth muscle phenotyping. Insulin (1 microM) was mitogenic for bovine tracheal smooth muscle and potentiated DNA-synthesis induced by other growth factors.

Muscarinic M3-receptors mediate cholinergic synergism of mitogenesis in airway smooth muscle.

Muscarinic receptor agonists have been considered to act synergistically in combination with growth facors on airway smooth muscle growth. Characterization of the proliferative responses and of the receptor subtype(s) involved has not yet been studied. Therefore, we investigated mitogenesis induced by stimulation of muscarinic receptors, alone and in combination with stimulation by platelet-derived growth factor (PDGF).

Functional characterization of serum- and growth factor-induced phenotypic changes in intact bovine tracheal smooth muscle.

1. The present study aims to investigate whether phenotypic changes, reported to occur in cultured isolated airway smooth muscle (ASM) cells, are of relevance to intact ASM. Moreover, we aimed to gain insight into the signalling pathways involved.