Index Of Cell Size Research Articles

Ethanol-induced skeletal muscle myopathy: biochemical and histochemical measurements on type I and type II fibre-rich muscles in the young rat.

Rats were pair-fed either a nutritionally complete liquid diet containing 36% of total calories as ethanol or isovolumetric amounts of the same diet in which ethanol was substituted by isocaloric glucose. Chronic ethanol feeding caused a preferential decline in the wet weight of the plantaris (predominantly Type II muscle fibres) which was accompanied by a reduction in the total DNA content. The soleus (a predominantly Type I fibre muscle) was relatively unaffected. Chronic ethanol exposure had no effect on the biochemical index of cell size (protein/DNA ratio) in either the plantaris or soleus. Quantitative histochemistry of Type II fibres in the plantaris demonstrated that ethanol caused an increase in the proportion of fibres with smaller diameters. Similar effects were observed for Type II fibres in the soleus. In contrast, ethanol exposure was associated with an increase in the relative proportion of Type I fibres with higher diameters, in both plantaris and soleus. Light microscopic examination of myopathic muscle sections demonstrated that lesions occurred without evidence of inflammation, fibrosis or other infiltration by non-muscle cells. It is concluded that chronic exposure of rats to ethanol is associated with skeletal muscle atrophy. The lesion appears to be specific for Type II fibres, irrespective of the predominant fibre type in the particular muscle.

Transforming growth factor-beta-induced growth inhibition and cellular hypertrophy in cultured vascular smooth muscle cells.

We have explored the hypothesis that hypertrophy of vascular smooth muscle cells may be regulated, in part, by growth inhibitory factors that alter the pattern of the growth response to serum mitogens by characterizing the effects of the potent growth inhibitor, transforming growth factor-beta (TGF-beta), on both hyperplastic and hypertrophic growth of cultured rat aortic smooth muscle cells. TGF-beta inhibited serum-induced proliferation of rat aortic smooth muscle cells (ED50 = 2 pM); this is consistent with previously reported observations in bovine aortic smooth muscle cells (Assoian et al. 1982. J. Biol. Chem. 258:7155-7160). Growth inhibition was due in part to a greater than twofold increase in the cell cycle transit time in cells that continued to proliferate in the presence of TGF-beta. TGF-beta concurrently induced cellular hypertrophy as assessed by flow cytometric analysis of cellular protein content (47% increase) and forward angle light scatter (32-50% increase), an index of cell size. In addition to being time and concentration dependent, this hypertrophy was reversible. Simultaneous flow cytometric evaluation of forward angle light scatter and cellular DNA content demonstrated that TGF-beta-induced hypertrophy was not dependent on withdrawal of cells from the cell cycle nor was it dependent on growth arrest of cells at a particular point in the cell cycle in that both cycling cells in the G2 phase of the cell cycle and those in G1 were hypertrophied with respect to the corresponding cells in vehicle-treated controls. Chronic treatment with TGF-beta (100 pM, 9 d) was associated with accumulation of cells in the G2 phase of the cell cycle in the virtual absence of cells in S phase, whereas subsequent removal of TGF-beta from these cultures was associated with the appearance of a significant fraction of cycling cells with greater than 4c DNA content, consistent with development of tetraploidy. Results of these studies support a role for TGF-beta in the control of smooth muscle cell growth and suggest that at least one mechanism whereby hypertrophy and hyperploidy may occur in this, as well as other cell types, is by alterations in the response to serum mitogens by potent growth inhibitors such as TGF-beta.

Cell death of motoneurons in the chick embryo spinal cord. VII. The survival of brachial motoneurons in dystrophic chickens

Motoneurons in the brachial lateral motor column (LMC) of the chicken were evaluated quantitatively from embryonic day (E) 6 to 3 weeks posthatching. Embryos from the dystrophic line 413 and the control line 412 were both found to have an extensive, naturally occurring loss of motoneurons between E6 and E16. The numerical extent of this loss was similar in both lines and amounted to approximately 50% of the original population that was present on E6. At no time during development was there a significant numerical difference in motoneurons between the dystrophic and control chickens. Neither the nuclear diameter, an index of cell size, nor the number of nucleoli per cell was found to differ between the two lines. Finally, treatment of embryos from E6 to E10 with a curare regimen sufficient to induce a sustained paralysis resulted in a quantitatively similar reduction in naturally occurring neuron death in both the dystrophic and control lines. Avian muscular dystrophy is not associated with an alteration in motoneuron survival. An experimental perturbation of neuromuscular interactions by chronic treatment with curare does not differentially affect motoneuron survival in control and dystrophic chickens.

Response to Nutritional Deprivation in the Japanese Quail (Coturnix Coturnix Japonica)

The accumulation of total tissue DNA as an index of cell number, and the weight/DNA ratio as an index of cell size were used to establish the effects of severe stunting imposed by malnutrition on cellular development and the permanence or reversibility of such stunting in Japanese quail. The results indicated that in the quail cellular growth is much more a function of hyperplastic growth than hypertrophy of existing cells and that, contrary to observations in the rat, hyperplastic growth is resumed after periods of underfeeding once an adequate supply of nutrients is provided. This suggests that in the quail the lesion created by nutritional stress is at the level of DNA synthesis. On a employé l’accumulation de l’ADN total des tissus comme indice du nombre de cellules et la rapport poids / ADN comme indice de la taille des cellules pour démontrer les effets d’un sévère arrêt de croissance imposé par malnutrition au développement cellulaire et la permanence ou la réversibilité d’un tel arrêt chez la caille du Japon. Les résultats ont montré que chez la caille la croissance cellulaire est plus fonction d’une croissance hyperplastique que d’une hypertrophie des cellules existantes et que contrairement aux observations faites chez le rat, la croissance hyperplastique reprend après des périodes de sous-alimentation une fois que les aliments sont fournis en quantité suffisante. Cela indique que la lésion créée chez la caille par suite d’une insuffisance alimentaire se fait au niveau de la synthèse de l’ADN. Man benutzt die Gesamtmenge der Gewebe-DNA als Index der Zellenzahl und das Verhältnis von Gewicht zur DNA als Index der Gesamtgrösse, um den durch die Wirkung der Unterernährung auf die Zellenentwicklung verursachten Zwergwuchs festzustellen und das Bestehenbleiben oder Vorübergehen solchen Zwergwuchses bei der japanischen Wachtel. Die Ergebnisse zeigten, dass hier das Zellenwachstum mehr eine Funktion des hyperplastischen Wuchses als eine Hypertrophie existierender Zellen ist und dass, im Gegensatz zu Beobachtungen bei Ratten, hyperplastisches Wachstum nach Hungerperioden wieder beginnt, sobald eine ausreichende Zufuhr von Nahrung vorhanden ist. Dies lässt darauf schliessen, dass die bei der Wachtel durch Hunger verursachte Störung sich in der DNA Synthese abspielt. A fin de establecer los efectos de la falta de desarrollo grave impuesta por la malnutrición sobre el desarrollo celular y la permanencia o reversibilidad de tal falta de crecimiento en la codorniz japonesa se utilizaron el acúmulo total de DNA corno índice de número celular y la razón peso/DNA como índice de todos los tamaños. Los resultados indican que el crecimiento celular la codorniz se encuentra en función mucho más del crecimiento de hiperplásico que del hipertrófico de las células existentes y que, al contrario de lo que sucede en las ratas, el crecimiento hiperplásico se reestablece de neuvo después de períodos más o menos largos de malnutrición una vez que se proporciona un suministro adecuado de substancias nutritivas. Esto sugiere que en la codorniz las lesiones pro ducidas por un stress nutritivo se producen a nivel de la síntesis del DNA.