PubMed Health⌕ Search

Biomedical subjects

J H Chamley-Campbell

Publications and source records attributed to J H Chamley-Campbell.

6 recordsLinked to original sources
PubMed1985

Tropic interactions between sympathetic nerves and vascular smooth muscle.

Explants of sympathetic ganglia from 3-9 day old rats were grown on collagen-coated coverslips in modified Rose chambers for 5 days, either alone or 2 mm away from explants of 6 week old rat caudal artery and aorta. Nerve fibre growth was stimulated on the side of the ganglion explant near the caudal artery explants but was not stimulated near the aorta. To determine the source of the nerve growth stimulation, explants of whole intact wall of the caudal artery, separated adventitia and medial layers, enzyme-dispersed cells, homogenized cells and medium pre-conditioned by caudal artery explants, were combined with ganglia. Explants of whole caudal artery and dispersed cells were also precultured prior to combination with ganglia. These combinations allowed analysis of the role of smooth muscle cells, existing nerve fibres, necrotic cells and connective tissue. Results suggested that degenerating nerve fibres within the blood vessels caused the increase in the number and the 'attraction' of the nerve fibres growing from the sympathetic ganglia. In contrast, both caudal artery and aorta from 3-9 day old rats caused stimulation of nerve fibre growth. Since these vessels were not yet innervated, the effect cannot be due to degenerating nerve terminals and a different mechanism must be involved.

Adrenergic Fibers↗
PubMed1981

Smooth muscle phenotypic modulation: role in atherogenesis.

Observations in vivo and in vitro demonstrate: 1) smooth muscle cells are capable of more than one function and can alter their phenotype/state accordingly (modulation); 2) in the majority of cases before a smooth muscle can divide it must modulate from a contractile to a synthetic phenotype; 3) modulation is reversible; 4) however, if synthetic state smooth muscle which has been stimulated to divide achieves approximately nine cell doublings before being inhibited by confluence it appears unable to return to the contractile state; 5) smooth muscle cells in the synthetic state respond almost immediately to serum mitogens and have an altered ability to metabolize low density lipoprotein compared with those in the contractile state 6) diffuse intimal thickenings and intimal cushions at branch points form from the media apparently as a result of adaptation of the vessel wall to growth and development and are sites of predilection for the formation of atherosclerotic plaques. The "smooth muscle metabolic reactivity" hypothesis of atherogenesis suggests that due to the large number of smooth muscle cell doublings which occur in the formation of diffuse intimal thickenings and intimal cushions at branch points a number of these cells are permanently in the synthetic state. This confers upon these cells a selective proliferative advantage and an altered ability to metabolize lipoproteins - both essential ingredients in atherogenesis.

Animals↗
PubMed1981

Phenotype-dependent response of cultured aortic smooth muscle to serum mitogens.

Smooth muscle cells from the aortic media of adult pigs and monkeys have been grown in primary culture by plating cells enzymatically dissociated from the intact aorta. During the first 6 d these cells are in the "contractile" phenotype. That is, they contract slowly in response to angiotensin II and their cytoplasm is filled with both thick and thin myofilaments. In this state they do not incorporate [3H]thymidine into DNA or proliferate in response to normolipemic or hyperlipemic whole blood serum (WBS). After 7 d in culture the cells undergo a spontaneous modulation of phenotype to a "synthetic" state where they cannot be stimulated to contract and their cytoplasm is filled with organelles usually associated with synthesis of secretory protein. Thick myosin-containing filaments can no longer be demonstrated. When challenged with normolipemic or hyperlipemic WBS the cells incorporate [3H]thymidine into DNA and undergo logarithmic growth. It is suggested that when smooth muscle is the contractile phenotype (as normally exists for most cells in the aortic media of adult animals) it does not divide when challenged with serum mitogens but can undergo a change of phenotype to a synthetic state in which division can be stimulated.

Animals↗
PubMed1978

Evidence for the presence of non-muscle actin in LW13K2 rat neoplastic cells.

It was demonstrated that I-bands in cultured cardiac muscle cells and non-interrupted fibrils in smooth muscle cells, irrespective of phenotypic state and number of subculture, stained with an antibody directed against native actin from chicken gizzard smooth muscle, but that non-muscle cells in the same cultures did not stain. Neoplastic rat LW13K2 cells, whether confluent or subconfluent, did not stain with the same muscle-actin antibody. This is by no means evidence of a non-muscle origin of LW13K2 cells. However, it does show that these cells express in culture an actin which is not the same as that in muscle cells, and consequently that it can be used as a source of non-muscle actin.

Actins↗
PubMedDate not supplied

What controls smooth muscle phenotype?

Enzyme-dispersed smooth muscle cells from the adult pig aortic media in the first few days of primary culture are in the contractile phenotype and do not divide when challenged with 5% WBS. After 6--8 days the isolated cells spontaneously undergo a change in phenotype where contraction cannot be stimulated and the cells respond to mitogens in WBS by logarithmic growth. The change in phenotype is reversible if the cells are seeded sufficiently densely (5 x 10(4) to 1 x 10(5)/ml) that a confluent monolayer results after less than 1 week of proliferation, but is irreversible if the cells are seeded sparsely (1 x 10(3) to 5 x 10(3)/ml) and take more than 2 weeks of proliferation to reach confluence. When the cells are seeded so densely (10(6)/ml) that a confluent monolayer is present from day 1, the cells do not undergo a change in phenotype but remain indefinitely in the contractile state. The spontaneous modulation of phenotype of isolated smooth muscle cells can be inhibited by a confluent monolayer of contractile smooth muscle or endothelial cells in co-culture with the sparsely seeded smooth muscle such that the two cell layers are not in contact but bathed by the same nutrient medium. Smooth muscle modulation can also be inhibited by a factor extracted from pig and rabbit aortic tissue, and its effects mimicked by commercially available sodium heparin at 50 units/ml.

Animals↗