| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| L J De Windt, H W Lim, T Taigen, D Wencker, G Condorelli, G W Dorn, R N Kitsis, J D Molkenti. Calcineurin-mediated hypertrophy protects cardiomyocytes from apoptosis in vitro and in vivo: An apoptosis-independent model of dilated heart failure. Circulation research. vol 86. issue 3. 2000-03-16. PMID:10679475. |
however, utilizing multiple approaches, we determined that calcineurin-mediated hypertrophy protected cardiac myocytes from apoptosis, suggesting a model of heart failure that is independent of apoptosis. |
2000-03-16 |
2023-08-12 |
mouse |
| L J De Windt, H W Lim, T Taigen, D Wencker, G Condorelli, G W Dorn, R N Kitsis, J D Molkenti. Calcineurin-mediated hypertrophy protects cardiomyocytes from apoptosis in vitro and in vivo: An apoptosis-independent model of dilated heart failure. Circulation research. vol 86. issue 3. 2000-03-16. PMID:10679475. |
adcna infection, which induced myocyte hypertrophy and atrial natriuretic factor expression, protected against apoptosis induced by 2-deoxyglucose or staurosporine, as assessed by terminal deoxynucleotidyltransferase-mediated dutp nick end labeling (tunel) labeling, caspase-3 activation, dna laddering, and cellular morphology. |
2000-03-16 |
2023-08-12 |
mouse |
| D V Messadi, A Le, S Berg, A Jewett, Z Wen, P Kelly, C N Bertolam. Expression of apoptosis-associated genes by human dermal scar fibroblasts. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. vol 7. issue 6. 2000-03-02. PMID:10633011. |
the purpose of this study was to determine if aberrant apoptosis plays a role in pathologic wound healing as manifested by hypertrophic scarring and keloid formation. |
2000-03-02 |
2023-08-12 |
human |
| G Silvestrini, P Ballanti, F R Patacchioli, P Mocetti, R Di Grezia, B M Wedard, L Angelucci, E Bonucc. Evaluation of apoptosis and the glucocorticoid receptor in the cartilage growth plate and metaphyseal bone cells of rats after high-dose treatment with corticosterone. Bone. vol 26. issue 1. 2000-01-20. PMID:10617155. |
the main results of the cort treatment were: a significant increase in apoptotic osteoblasts, and a concomitant decrease in the histomorphometric variables of bone formation, with a reversal of both values during recovery; a nonsignificant increase in the apoptosis of osteoclasts, without changes in the histomorphometric variables of bone resorption; a significant increase in apoptotic terminal hypertrophic chondrocytes; the presence of gr in all types of skeletal cells in control rats, with different (cytoplasmic and/or nuclear) immunohistochemical detection in the same type of cell; a decrease in gr detection in proliferative chondrocytes and osteocytes in cort and recovery groups, and in the maturative/hypertrophic chondrocytes of the recovery group; a fall in growth cartilage width, possibly due to the reduced proliferation of proliferative chondrocytes and increased apoptosis in terminal hypertrophic chondrocytes. |
2000-01-20 |
2023-08-12 |
rat |
| G Silvestrini, P Ballanti, F R Patacchioli, P Mocetti, R Di Grezia, B M Wedard, L Angelucci, E Bonucc. Evaluation of apoptosis and the glucocorticoid receptor in the cartilage growth plate and metaphyseal bone cells of rats after high-dose treatment with corticosterone. Bone. vol 26. issue 1. 2000-01-20. PMID:10617155. |
in conclusion, pharmacological doses of cort reduce bone formation by increasing osteoblast apoptosis; they reduce growth cartilage width, probably by inhibiting chondrocyte proliferation and increasing the apoptosis of terminal hypertrophic chondrocytes, and they reduce osteocyte gr. |
2000-01-20 |
2023-08-12 |
rat |
| P Preisi. A cell cycle-dependent mechanism of renal tubule epithelial cell hypertrophy. Kidney international. vol 56. issue 4. 1999-12-02. PMID:10610409. |
the response of renal epithelial cells to injury can include hyperplasia (increase in cell number), apoptosis (cell death), antiproliferation (growth arrest), or hypertrophy (cells physically enlarge). |
1999-12-02 |
2023-08-12 |
Not clear |
| Y Ono, H Ono, H Matsuoka, T Fujimori, E D Frohlic. Apoptosis, coronary arterial remodeling, and myocardial infarction after nitric oxide inhibition in SHR. Hypertension (Dallas, Tex. : 1979). vol 34. issue 4 Pt 1. 1999-12-01. PMID:10523335. |
in addition, we evaluated whether the development of coronary arterial smooth muscular cell apoptosis was related to hemodynamics or to vascular hypertrophy. |
1999-12-01 |
2023-08-12 |
rat |
| Y Ono, H Ono, H Matsuoka, T Fujimori, E D Frohlic. Apoptosis, coronary arterial remodeling, and myocardial infarction after nitric oxide inhibition in SHR. Hypertension (Dallas, Tex. : 1979). vol 34. issue 4 Pt 1. 1999-12-01. PMID:10523335. |
apoptosis occurred predominantly in hypertrophic coronary arterial smooth muscular cells; myocardial infarction and ventricular fibrosis were exacerbated by impaired hemodynamics induced by l-name. |
1999-12-01 |
2023-08-12 |
rat |
| A M Costa, S Peyrol, L C Pôrto, J P Comparin, J L Foyatier, A Desmoulièr. Mechanical forces induce scar remodeling. Study in non-pressure-treated versus pressure-treated hypertrophic scars. The American journal of pathology. vol 155. issue 5. 1999-11-30. PMID:10550323. |
our results show that, in hypertrophic scars, pressure therapy restores in part the extracellular matrix organization observed in normal scar and induces the disappearance of alpha-smooth muscle actin-expressing myofibroblasts, probably by apoptosis. |
1999-11-30 |
2023-08-12 |
Not clear |
| C E Herrman, R A Sanders, J E Klaunig, L R Schwarz, J B Watkin. Decreased apoptosis as a mechanism for hepatomegaly in streptozotocin-induced diabetic rats. Toxicological sciences : an official journal of the Society of Toxicology. vol 50. issue 1. 1999-10-19. PMID:10445763. |
this study examined hypertrophy, hyperplasia, and apoptosis, three basic aspects of tissue growth, in livers of sprague-dawley and wistar rats made diabetic by iv injection of streptozotocin 8, 30, or 90 days previously. |
1999-10-19 |
2023-08-12 |
rat |
| S Ikeda, M Hamada, K Hiwad. Contribution of non-cardiomyocyte apoptosis to cardiac remodelling that occurs in the transition from compensated hypertrophy to heart failure in spontaneously hypertensive rats. Clinical science (London, England : 1979). vol 97. issue 2. 1999-10-12. PMID:10409480. |
contribution of non-cardiomyocyte apoptosis to cardiac remodelling that occurs in the transition from compensated hypertrophy to heart failure in spontaneously hypertensive rats. |
1999-10-12 |
2023-08-12 |
rat |
| S Ikeda, M Hamada, K Hiwad. Contribution of non-cardiomyocyte apoptosis to cardiac remodelling that occurs in the transition from compensated hypertrophy to heart failure in spontaneously hypertensive rats. Clinical science (London, England : 1979). vol 97. issue 2. 1999-10-12. PMID:10409480. |
the aim of the present study is to clarify (1) whether cardiac apoptosis occurs during the transition from compensated hypertrophy to decompensated heart failure, and (2) whether expression of the genes encoding bax (an apoptosis inducer) and bcl-xl and bcl-2 (apoptosis inhibitors) is altered during this transition. |
1999-10-12 |
2023-08-12 |
rat |
| S Ikeda, M Hamada, K Hiwad. Contribution of non-cardiomyocyte apoptosis to cardiac remodelling that occurs in the transition from compensated hypertrophy to heart failure in spontaneously hypertensive rats. Clinical science (London, England : 1979). vol 97. issue 2. 1999-10-12. PMID:10409480. |
in conclusion, non-cardiomyocyte apoptosis may play a contributory role in the remodelling that occurs in the transition from compensatory hypertrophy to decompensated heart failure. |
1999-10-12 |
2023-08-12 |
rat |
| E H Sonnenblick, P Anvers. Models and remodeling: mechanisms and clinical implications. Cardiologia (Rome, Italy). vol 44. issue 7. 1999-10-08. PMID:10476585. |
involved in this process are hypertrophy, dilation, myocyte loss whether due to necrosis or apoptosis, and myocyte hyperplasia. |
1999-10-08 |
2023-08-12 |
Not clear |
| B Zerega, S Cermelli, P Bianco, R Cancedda, F D Cancedd. Parathyroid hormone [PTH(1-34)] and parathyroid hormone-related protein [PTHrP(1-34)] promote reversion of hypertrophic chondrocytes to a prehypertrophic proliferating phenotype and prevent terminal differentiation of osteoblast-like cells. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. vol 14. issue 8. 1999-09-30. PMID:10457260. |
the effects of parathyroid hormone/parathyroid hormone-related protein (pth/pthrp) on late events in chondrocyte differentiation were investigated by a dual in vitro model where conditions of suspension versus adhesion culturing are permissive either for apoptosis or for the further differentiation of hypertrophic chondrocytes to osteoblast- like cells. |
1999-09-30 |
2023-08-12 |
chicken |
| B Zerega, S Cermelli, P Bianco, R Cancedda, F D Cancedd. Parathyroid hormone [PTH(1-34)] and parathyroid hormone-related protein [PTHrP(1-34)] promote reversion of hypertrophic chondrocytes to a prehypertrophic proliferating phenotype and prevent terminal differentiation of osteoblast-like cells. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. vol 14. issue 8. 1999-09-30. PMID:10457260. |
these data indicate that pth/pthrp inhibit both the mineralization of a cartilage-like matrix and apoptosis (mimicked in the suspension culture) and the production of a mineralizing bone-like matrix, characterizing further differentiation of hypertrophic chondrocytes to osteoblasts like cells (mimicked in adhesion culture). |
1999-09-30 |
2023-08-12 |
chicken |
| M A Mello, R S Tua. High density micromass cultures of embryonic limb bud mesenchymal cells: an in vitro model of endochondral skeletal development. In vitro cellular & developmental biology. Animal. vol 35. issue 5. 1999-09-23. PMID:10475272. |
these findings showed that cellular differentiation, maturation, hypertrophy, calcification, and apoptosis occurred sequentially in the embryonic limb mesenchyme micromass cultures and indicate their utility as a convenient in vitro model to investigate the regulatory mechanisms of endochondral ossification. |
1999-09-23 |
2023-08-12 |
chicken |
| B S Tea, T V Dam, P Moreau, P Hamet, D deBloi. Apoptosis during regression of cardiac hypertrophy in spontaneously hypertensive rats. Temporal regulation and spatial heterogeneity. Hypertension (Dallas, Tex. : 1979). vol 34. issue 2. 1999-09-15. PMID:10454446. |
apoptosis during regression of cardiac hypertrophy in spontaneously hypertensive rats. |
1999-09-15 |
2023-08-12 |
rat |
| B S Tea, T V Dam, P Moreau, P Hamet, D deBloi. Apoptosis during regression of cardiac hypertrophy in spontaneously hypertensive rats. Temporal regulation and spatial heterogeneity. Hypertension (Dallas, Tex. : 1979). vol 34. issue 2. 1999-09-15. PMID:10454446. |
we previously reported that increased apoptosis participates in the regression of aortic hypertrophy in spontaneously hypertensive rats. |
1999-09-15 |
2023-08-12 |
rat |
| B S Tea, T V Dam, P Moreau, P Hamet, D deBloi. Apoptosis during regression of cardiac hypertrophy in spontaneously hypertensive rats. Temporal regulation and spatial heterogeneity. Hypertension (Dallas, Tex. : 1979). vol 34. issue 2. 1999-09-15. PMID:10454446. |
to further document the potential role of apoptosis in cardiovascular therapy, we examined apoptosis during regression of hypertrophy in the heart of spontaneously hypertensive rats receiving the antihypertensive drug enalapril (30 mg. kg(-1). |
1999-09-15 |
2023-08-12 |
rat |