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Biomedical subjects

M M Sholley

Publications and source records attributed to M M Sholley.

26 records · Page 2Linked to original sources
PubMed1978

Endothelial proliferation in inflammation. II. Autoradiographic studies in x-irradiated leukopenic rats after thermal injury to the skin.

The effect of leukocyte depletion on endothelial proliferation in the microvasculature of skin sites of acute inflammation was studied. Leukocytes were suppressed by 800 rad of whole-body irradiation 2 or 4 days prior to producing necrotizing thermal injuries (60 C, 20 seconds) on a shielded area of skin. Endothelial proliferation was assayed 3 days after thermal injury by quantitating the labeling index after injection of 3H-thymidine. Circulating mononuclear cells were depressed to 1.3% of pre-irradiation levels by 2 days and remained at similar levels at 5 days. Lesions developing over this interval were devoid of mononuclear infiltrate, although neutrophils emigrated as usual. Three-day lesions without mononuclear infiltrate had a mean endothelial-labeling index of 8.97%, and this was not significantly different control controls (9.42%). Lesions induced at 4 days, when circulating neutrophils were also suppressed, had reduced infiltration of neutrophils, but endothelial-labeling indexes were similar to those of controls. The results indicate that infiltration by monocytes is not a necessary stimulus for endothelial proliferation of new vessel growth in sites of nonimmunologic acute inflammation.

Animals↗
PubMed1977

Cellular migration and replication in endothelial regeneration: a study using irradiated endothelial cultures.

Cellular migration and replication were studied during repair of mechanical injuries produced in cultured monolayers of vascular endothelium. Human endothelial cells were obtained by collagenase perfusion of term umbilical cord veins and were grown on glass cover slips in replicate primary cultures. Following standardized mechanical denudation ("wounding") of narrow linear areas in postconfluent cultures, cellular migration and DNA synthesis were assessed at intervals after terminal 3H-thymidine incubation. Migration of cells from the edges of the wound into the denuded area was consistently underway by 12 hours, and by 24 hours there was considerable repopulation of the wound. A significant increase in 3H-thymidine labeling was not observed in the wound area until 36 hours. When cultures were exposed to 1500 rads of x-rays 1 hour prior to wounding, labeling was nearly abolished at 48 and 72 hours despite continuous incubation with 3H-thymidine. However, migration occurred as usual and resulted in repopulation similar to that in nonirradiated replicate cultures. These studies indicate that small endothelial defects can be significantly repaired by migration of adjacent viable cells. Thus, factors influencing both migration and replication should be considered in studies dealing with endothelial regeneration in vivo.

Cell Division↗
PubMed1977

Endothelial proliferation in the delayed hypersensitivity reaction: an autoradiographic study.

The time-sequence of endothelial proliferation in the delayed hypersensitivity reaction was examined in the skin of guinea pigs. Animals were sensitized to tuberculin (PPD) and dinitrochlorobenzene (DNCB) and skin lesions were examined 12 hr to 7 days after challenge. Thirty minutes before sacrifice 3H-thymidine (3H-T) was injected i.p. and endothelial labeling was assessed in autoradiographs of 1.5-mu thick methacrylate sections. Endothelial labeling became manifest at 24 hr (PPD) and 12 hr (DNCB) after challenge, reaching a peak at 48 to 72 hr in PPD-sensitized animals and 36 to 48 hr in DNCB-sensitized animals. Peak labeling indices were 7.88 and 15.08%, respectively. Labeling indices for nonsensitized control groups were always less than 1%. Endothelial labeling was associated, in time of occurrence, distribution, and magnitude with mononuclear cell infiltration of the lesions. These findings thus document the occurrence of significant endothelial cell proliferation in delayed hypersensitivity responses and suggest that the events leading to the expression of hypersensitivity also result in endothelial replication.

Animals↗
PubMed1977

Endothelial proliferation in inflammation. I. Autoradiographic studies following thermal injury to the skin of normal rats.

Endothelial prolifertion was studied in sites of acute inflammation induced by necrotizing (60 C for 20 seconds) or mild (54 C for 20 seconds) thermal injury to the skin of rsts. DNA synthesis in endothelial cells was assayed 6 hours to 10 days following injury by quantitation of the (3)H-thymidine labeling indices on 2-mu Epon section autoradiographs. In lesions induced at 60 C for 20 seconds, increase in DNA synthesis in small vessels around the necrotic tissue began at 1 day and became significant at 2 and 3 days (10 to 12% for endothelial cells, 9% for perivascular cells). This increased endothelial replication resulted in the formation of new blood vessels by 5 to 7 days. Endothelial labeling diminished progressively after 3 days, as the epidermis regenerated. Foci completely covered by new epidermis consistently showed lower labeling indices than those which were not reepithelialized. Mild thermal injury (54 C for 20 seconds) also resulted in significant increases in endothelial labeling (6%), but the labeling was present mainly in superficial vessels and was not followed by neovascularization. The findings with mild injury are consistent with data that vascular leakage from superficial vessels is due to direct, albeit delayed, endothelial damage. Electron microscopic studies confirmed labeling in endothelial cells and indicated that ultrastructural alterations that were previously ascribed to activation, recovery, or regenerative transformation of endothelium represent, in the main, endothelial proliferation.

Animals↗
PubMed1976

Endothelial DNA synthesis in themicrovasculature of rat skin during the hair growth cycle.

Earlier studies of the vascular patterns around hair follicles revealed that actively growing follicles have an extensive microvasculature relative to that around quiescent follicles. In order to determine whether the establishment of the active perifollicular vascular pattern involves replication of endothelial and perivascular cells, we studied the 3H-thymidine labeling indices of these cells in autoradiographs of rat skin from regions containing either actively growing follicles or recently inactive follicles. In skin containing inactive follicles, the endothelial labeling index was 0.22%, a figure similar to those reported for the endothelium of small blood vessels in several other non-stimulated adult tissues. However, skin containing actively growing follicles displayed an endothelial labeling index of 2.35%. The labeling indices of perivascular cells paralleled those of the endothelial cells. Thus, endothelial and perivascular cells in vessels associated with actively growing follicles undergo significantly more DNA synthesis than those in vessels associated with inactive follicles. Replication of these cells apparently contributes to the extension of the microvascular network around growing follicles.

Animals↗