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Biomedical subjects

H L Moses

Publications and source records attributed to H L Moses.

198 records · Page 11Linked to original sources
PubMed1968

Ultrastructural studies of vasopressin effect on isolated perfused renal collecting tubules of the rabbit.

Isolated cortical collecting tubules from rabbit kidney were studied during perfusion with solutions made either isotonic or hypotonic to the external bathing medium. Examination of living tubules revealed a reversible increase in thickness of the cellular layer, prominence of lateral cell membranes, and formation of intracellular vacuoles during periods of vasopressin-induced osmotic water transport. Examination in the electron microscope revealed that vasopressin induced no changes in cell structure in collecting tubules in the absence of an osmotic difference and significant bulk water flow across the tubule wall. In contrast, tubules fixed during vasopressin-induced periods of high osmotic water transport showed prominent dilatation of lateral intercellular spaces, bulging of apical cell membranes into the tubular lumen, and formation of intracellular vacuoles. It is concluded that the ultrastructural changes are secondary to transepithelial bulk water flow and not to a direct effect of vasopressin on the cells, and that vasopressin induces osmotic flow by increasing water permeability of the luminal cell membrane. The lateral intercellular spaces may be part of the pathway for osmotically induced transepithelial bulk water flow.

Animals↗
PubMedDate not supplied

Growth factors in the tumorigenicity of a brain tumor cell line.

We studied a virally induced canine gliosarcoma brain tumor cell line capable of producing brain tumors in vivo following intracerebral inoculation of the cells into the brains of adult mongrel dogs. Cloned populations from this cell line differed in their ability to produce brain tumors in vivo. In vitro transforming growth factor-beta secretion by each clone correlated with in vivo tumorigenicity. Mitogenic activity like that produced with platelet-derived growth factor was also secreted by each clone and correlated with in vivo tumorigenicity. Epidermal growth factor and transforming growth factor-alpha production was not detected in any of the clones of canine gliosarcoma cells. Although only some of the brain tumor cell clones were able to produce tumors in immunologically normal dogs, brain tumors were produced in all dogs pretreated with cyclosporin and in all "nude" mice, suggesting that tumor immunology plays an important role in this brain tumor model. In vitro cloning efficiency of each brain tumor cell clone also correlated with in vivo tumorigenicity. We postulate that transforming growth factor-beta may both stimulate brain tumor cell growth and inhibit host antitumor immune surveillance.

Animals↗
PubMedDate not supplied

Production and auto-induction of transforming growth factor-alpha in human keratinocytes.

Transforming growth factor-alpha (TGF-alpha) is a polypeptide which is structurally related to epidermal growth factor (EGF) and binds to the EGF receptor. TGF-alpha synthesis occurs in a variety of neoplastic cells and during early fetal development but has not been reported in normal cells of the adult organisms. TGF-alpha has therefore been regarded as an embryonic growth factor which is inappropriately expressed during neoplasia. Here we report that primary cultures of normal human keratinocytes synthesize TGF-alpha. Furthermore, we show that addition of EGF or TGF-alpha to these cultures induces TGF-alpha gene expression, suggesting that a mechanism of auto-induction exists. Analysis of normal skin biopsies using in situ hybridization and immunohistochemistry demonstrates the in vivo presence of TGF-alpha messenger RNA and protein in the stratified epidermis.

Cells, Cultured↗
PubMedDate not supplied

Mechanisms of transforming growth factor-beta 1-induced cell cycle arrest.

Mitogenic stimulation of normal cells initiates a sequence of events leading to activation of cyclin-dependent kinases, phosphorylation of Rb, and subsequent entry of the cell into the S phase. Evidence is accumulating that transforming growth factor-beta 1 (TGF beta 1) inhibits cell cycle progression by blocking a number of steps involved in cdk activation, thus preventing the massive phosphorylation of Rb in late G1. Many types of cancer have lost sensitivity to the growth-inhibitory actions of TGF beta 1, which is thought to be an important step in the process of oncogenic transformation. Recent findings suggest that in many cancers TGF beta 1 insensitivity may result from disregulated expression of cyclin, cdk, and cdk inhibitor genes. These alterations allow inappropriate cdk activation and Rb phosphorylation, resulting in inactivation of the growth suppressive functions of Rb and uninhibited S phase entry. Further work will be needed to clarify the mechanisms of cdk inhibition by TGF beta 1 and how these events are linked to TGF beta 1 receptor-ligand binding and signaling.

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