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Cell Hypertrophy (cell + hypertrophy)
Selected AbstractsThyroid hormone-mediated growth and differentiation of growth plate chondrocytes involves IGF-1 modulation of ,-catenin signalingJOURNAL OF BONE AND MINERAL RESEARCH, Issue 5 2010Lai Wang Abstract Thyroid hormone regulates terminal differentiation of growth plate chondrocytes in part through modulation of the Wnt/,-catenin signaling pathway. Insulin-like growth factor 1 (IGF-1) has been described as a stabilizer of ,-catenin, and thyroid hormone is a known stimulator of IGF-1 receptor expression. The purpose of this study was to test the hypothesis that IGF-1 signaling is involved in the interaction between the thyroid hormone and the Wnt/,-catenin signaling pathways in regulating growth plate chondrocyte proliferation and differentiation. The results show that IGF-1 and the IGF- receptor (IGF1R) stimulate Wnt-4 expression and ,-catenin activation in growth plate chondrocytes. The positive effects of IGF-1/IGF1R on chondrocyte proliferation and terminal differentiation are partially inhibited by the Wnt antagonists sFRP3 and Dkk1. T3 activates IGF-1/IGF1R signaling and IGF-1-dependent PI3K/Akt/GSK-3, signaling in growth plate chondrocytes undergoing proliferation and differentiation to prehypertrophy. T3 -mediated Wnt-4 expression, ,-catenin activation, cell proliferation, and terminal differentiation of growth plate chondrocytes are partially prevented by the IGF1R inhibitor picropodophyllin as well as by the PI3K/Akt signaling inhibitors LY294002 and Akti1/2. These data indicate that the interactions between thyroid hormone and ,-catenin signaling in regulating growth plate chondrocyte proliferation and terminal differentiation are modulated by IGF-1/IGF1R signaling through both the Wnt and PI3K/Akt signaling pathways. While chondrocyte proliferation may be triggered by the IGF-1/IGF1R-mediated PI3K/Akt/GSK3, pathway, cell hypertrophy is likely due to activation of Wnt/,-catenin signaling, which is at least in part initiated by IGF-1 signaling or the IGF-1-activated PI3K/Akt signaling pathway. © 2010 American Society for Bone and Mineral Research [source] An Autopsy Case of Brugada Syndrome with Significant Lesions in the Sinus NodeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 3 2005SHIN-ICHIRO MORIMOTO M.D. A 30-year-old man with Brugada syndrome died suddenly. The heart weighed 380 g. The left ventricular wall showed mild thickening, and marked fatty tissue deposition was noted in the right ventricular outflow tract. Neither ventricle was enlarged. Contraction band necrosis was diffuse in both ventricles. In the ventricles no cardiac muscle cell hypertrophy or atrophy, or significant interstitial fibrosis was observed. In the sinus node the number of nodal cells was reduced by half, with fatty tissue and fibrosis prominent. But no lesions were evident in the right bundle branch. [source] Aging-Related Increase to Inducible Atrial Fibrillation in the Rat ModelJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2002HIDEKI HAYASHI M.D. Aging and Atrial Fibrillation.Introduction: Aging is associated with atrial interstitial fibrosis and increased incidence of atrial fibrillation (AF). We hypothesized that aged rats are suitable for study of aging-related AF and that partial atrial cellular uncoupling induced with heptanol in young rats mimics aging-related AF. Methods and Results: Interatrial conduction time and atrial response to burst atrial pacing were evaluated in 11 young (2,3 months) and 12 old (22,24 months) male rats (Fisher 344) in the Langendorff-perfused setting. At baseline, sustained (>30 sec) atrial tachycardia (AT) and AF were induced in 10 of 12 and in 7 of 12 old rats, respectively. No such arrhythmias could be induced in the young rats. Old rats had significantly (P < 0.01) longer interatrial conduction time and P wave durations than the young rats. Burst pacing failed to induce AT and AF in all 11 young rats studied. The effects of heptanol 2 to 10 ,M were studied in both groups. Heptanol 2 to 5 ,M promoted inducible AT in all 5 young rats studied; however, when its concentration was raised to 10 ,M, AT could no longer be induced in any of the 5 young rats. No AF could be induced in any of the 5 young rats at heptanol concentrations of 2 to 10 ,M. In the old rats, AF could still be induced during perfusion of 2 ,M heptanol. However, when its concentration was raised to 5 and 10 ,M, AF could not be induced in any of the 6 old rats studied. Optical mapping using a potentiometric dye showed a periodic single wavefront of activation during AT in both groups and 2 to 4 independent wavefronts propagating in different directions during AF in the old rats. Histology revealed a significant increase in interstitial atrial fibrosis (P < 0.01), atrial cell size (P < 0.05), and heart weight in old versus young rats. Fibrosis in the old rats was highly heterogeneous. Conclusion: The rat model is suitable for study of aging-related AF. Uniform partial atrial cellular uncoupling with heptanol perfusion in the young rats, although promoting inducible AT, does not mimic aging-related AF. The results suggest that heterogeneous atrial interstitial fibrosis and atrial cell hypertrophy might contribute to the aging-related increase in atrial conduction slowing, conduction block, and inducible AF in the old rat model. [source] Ageing of substantia nigra in humans: cell loss may be compensated by hypertrophyNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 4 2002C. R. Cabello In a stereological study of the human substantia nigra (SN), the total number of melanin-positive and melanin-negative neurones from 28 male subjects aged 19,92 years was estimated using a uniform sampling design and optical disectors. There was a significant decrease in the total number of melanin-positive neurones as a function of age (r2=0.18, residual-CV=0.35, 2P=0.032). Using the rotator method, the size distribution of the melanin-positive neurones was estimated and showed a significant difference in mean cell volume of melanin-positive neurones between the seven youngest (21,077 µm3) and the seven oldest individuals (32,011 µm3), 2P=0.022. Using a combination of the total number of melanin-positive neurones and their size distribution, the total perikaryon volume of melanin-positive neurones could be estimated and showed no decrease with increasing age (r2=0.01, residual-CV=0.41, 2P=0.62). Age-related decline in dopamine-transporter neurones within the SN might explain the occurrence of extrapyramidal symptoms in many elderly individuals. Although age-related cell hypertrophy is usually considered to be an indication of cell degeneration or necrosis, this might not always be the case. The fact that motor symptoms, although present in many of the elderly, are of a limited nature despite the high percentage of lost neurones could be due to a compensatory increase in the cell body of dopamine-producing SN neurones. Thus, the total amount of cell substance capable of producing the essential transmitters might not be reduced to a critically low level as a result of ageing. [source] Degeneration of germ line cells in amphibian ovaryACTA ZOOLOGICA, Issue 3 2010Maria Ogielska Abstract Ogielska, M., Rozenblut, B., Augusty,ska, R., Kotusz, A. 2010. Degeneration of germ line cells in amphibian ovary. ,Acta Zoologica (Stockholm) 91: 319,327 We studied the morphology of degenerating ovarian follicles in juvenile and adult frogs Rana temporaria, Rana lessonae and Rana ridibunda. Degeneration of primordial germ cells was never observed and was extremely rare in oogonia and early oocytes in a cyst phase in juveniles. Previtellogenic oocytes were rarely affected. Three main types of atresia were identified. In type I (subdivided into stages A,D), vitellogenic oocytes are digested by proliferating follicle cells that hypertrophy and become phagocytic. A , germinal vesicle shrinks, nucleoli fuse, oocyte envelope interrupts, and follicular cells hypertrophy; B , follicular cells multiply and invade the oocyte; C , entire vesicle is filled by phagocytic cells; D , degenerating phagocytes accumulate black pigment. Type II is rare and resembles breakdown of follicles and release of ooplasm. In type III, observed in previtellogenic and early vitellogenic oocytes, ooplasm and germinal vesicle shrink, follicle cells do not invade the vesicle, and condensed ooplasm becomes fragmented. The residual oogonia in adult ovaries (germ patches) multiply, but soon degenerate. [source] Ultrastructure of the ovary and oogenesis in six species of patellid limpets (Gastropoda: Patellogastropoda) from South AfricaINVERTEBRATE BIOLOGY, Issue 3 2000Alan N. Hodgson Abstract. The ultrastructural features of the ovary and oogenesis have been described in 6 species of patellid limpets from South Africa. The ovary is a complex organ that is divided radially into numerous compartments or lacunae by plate-like, blind-ended, hollow trabeculae that extend from the outer wall of the ovary to its central lumen. Trabeculae are composed of outer epithelial cells, intermittent smooth muscle bands, and extensive connective tissue. Oocytes arise within the walls of the trabeculae and progressively bulge outward into the ovarian lumen during growth while partially surrounded by squamous follicle cells. During early vitellogenesis, the follicle cells lift from the surface of the underlying oocytes and microvilli appear in the perivitelline space. Follicle cells restrict their contact with the oocytes to digitate foot processes that form desmosomes with the oolamina. When vitellogenesis is initiated, the trabecular epithelial cells hypertrophy and become proteosynthetically active. Yolk synthesis involves the direct incorporation of extraoocytic precursors from the lumen of the trabeculae (hemocoel) into yolk granules via receptor-mediated endocytosis. Lipid droplets arise de novo and Golgi complexes synthesize cortical granules that form a thin band beneath the oolamina. A fibrous jelly coat forms between the vitelline envelope and the overlying follicle cells in all species. [source] | |||||||||||||