DNA in the rat uterus myometrium during pregnancy and postpartum involution

Afting, E G; Elce, John S.

doi:10.1016/0003-2697(78)90321-4

Cited by 25 publications

(14 citation statements)

References 25 publications

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“…Physiological organ involution through apoptosis occurs in the uterus post partum (Afting & Elce, 1978). In a single experiment, in rat uteri 2 days post partum about 70 apoptotic bodies among 14,000 cells scored were found, 67% of them stained positive for pre(266-278) TGF-pl; no or only a weakly positive reaction was observed with anti LC(I-30).…”

Section: Resultsmentioning

confidence: 95%

Transforming growth factor-β 1 as a signal for induction of cell death by apoptosis

Bursch

Oberhammer²,

Jirtle³

et al. 1993

Br J Cancer

162

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The pathogenesis of tumours in the liver and other organs has been found to include disturbance of mechanisms controlling cell death by apoptosis (Bursch et al., 1984;Columbano et al., 1984; Garcea et al., 1984;Wyllie, 1985; SchulteHermann et al., 1990;Henderson et al., 1991). Our previous studies on the regulation of liver growth revealed that apoptosis serves to eliminate hepatocytes during involution of hormonally induced liver hyperplasia and during carcinogenesis in preneoplastic tissues (Bursch et al., 1984; SchulteHermann et al., 1990). Tumour promoters inhibit apoptosis, thereby accelerating growth of preneoplastic lesions and occurrence of frank neoplasia in the liver (Bursch et al., 1984;Schulte-Hermann et al., 1990). Furthermore, in hormonedependent tumours massive apoptosis can be induced by hormone withdrawal or by hormone antagonists, resulting in rapid tumour regression (Kyprianou et al., 1990;Szende et al., 1990;Bursch et al., 1991). Therefore elucidation of signal factors that can initiate apoptosis in hyperplastic and neoplastic tissues would be of great importance. Up to now progess in understanding the regulation of apoptosis was mainly restricted to hematological cells (Wyllie et al., 1980;Duke & Cohen, 1986;Trauth et al., 1989;Savill et al., 1990;Williams et al., 1990;Koury & Bondurant, 1990;Nunez et al., 1990).In epithelial tissues TGF-,11 was found to be a negative regulator of growth. It inhibits DN-A synthesis in liver (Carr et al., 1986;Russell et al., 1988), mammary gland (Coletta et al., 1991), uterine endometrium (Rotello et al., 1991) etc. In whole organ homogenates from prostate regressing after castration and from regressing tumours enhanced expression of TGF-,1I was found suggesting its involvement in apoptosis (Kyprianou et al., 1990;Kyprianou & Isaacs, 1989). In primary cultures of uterine endometrial cells and of hepatocytes TGF-,1I induced cell death (Rotello et al., 1991;Oberhammer et al., 1991). In the present study we asked whether TGF-P1 can be detected in individual dying cells of involuting tissues in vivo using immunohistochemical techniques with antibodies raised against two synthetic peptides of the molecule. The first corresponds to the amino terminals 30 amino acids of mature TGF-P1 (LC(1-30)), the second to amino acids 266-278 of the TGF-P1 precursor Flanders et al., 1989 Furthermore, in cultured primary hepatocytes, TGF-P1 is shown to be an inducer of apoptosis. In conclusion, the present study strongly suggests the involvement of TGF-P1 in

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Section: Resultsmentioning

confidence: 95%

Transforming growth factor-β 1 as a signal for induction of cell death by apoptosis

Bursch

Oberhammer²,

Jirtle³

et al. 1993

Br J Cancer

162

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“…As rapidly as possible, the uteri were removed, pinned to a cork board, lightly blotted, freed of fat and other tissue, cut open lengthwise, and the products of conception were removed. The uterine tissue was not otherwise cut or scraped, so that the endometrial layer was included in subsequent extracts, in contrast with our earlier practice [14]. The wet weight of the uterus was recorded, and samples were taken for the various assays.…”

Section: Tissue Preparationmentioning

confidence: 99%

“…These results led us to investigate the regulation of calpain synthesis during pregnancy, measuring calpain protein by immunochemical means and mRNA by means of nucleic acid probes that we have recently isolated for the calpains. The rat uterus undergoes a rapid and roughly 10-fold increase in wet weight during pregnancy, in a period of 21 days, and an even more rapid involution within 5-6 days post partum [14]. It therefore provides a useful model of complex hormonal regulation of growth, without any need for possibly unphysiological intervention.…”

Section: Introductionmentioning

confidence: 99%

Constitutive expression of calpain II in the rat uterus during pregnancy and involution

Samis

Back

Graham

et al. 1991

Biochemical Journal

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Partial genomic clones for the 80 kDa subunits of rat calpains I and II have been isolated. Some exons have been located and sequenced, and used to synthesize RNA probes specific for each isoenzyme. The levels of total DNA, soluble protein, calpain II 80 kDa subunit and the mRNA for this subunit were measured in parallel in separate extracts of non-pregnant, pregnant and post-partum rat uteri. The amount of total DNA, expressed as mg/g wet wt. of tissue, was found to remain constant throughout this period, except for a slight rise during involution. Calpain I was present in all samples in very small amounts. The amounts of calpain II 80 kDa subunit (measured on immunoblots) and of its mRNA (measured by means of slot-blots) also did not vary, when expressed in terms of units per g wet wt., during the 10-fold growth of the uterus during pregnancy and its post-partum involution. It was concluded that expression of calpain II was constitutive in this normal tissue, which is undergoing rapid growth and involution under complex hormonal control.

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“…So intense transformations indicate potent adaptive potentialities of the uterine tissues and appreciable velocity of the biological processes providing these changes under physiological conditions. The weight of the uterine myometrium increases at the expense of the size and number of smooth-muscle cells (SMC) [4], the contribution of each of these processes being about the same. Postpartum involution of the myometrium is presumably realized through the following intracellular mechanisms: myocyte clasmatosis leading to cell shrinkage [7], autophagocytosis (occurring mainly in the fibroblasts) [6], and apoptosis surely eventuating in cell elimination [8].…”

mentioning

confidence: 99%

Structural Transformations of Myocytes during Gestation and Early Postpartum Involution of the Uterus

2008

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Myocytes with large homogeneous vacuoles and numerous protrusions of the cytoplasm into extracellular space (manifestations of clasmatosis) were detected in rat myometrium during normal gestation and early postpartum period. The percentage of vacuolated smooth-muscle cells and numerical density of inflammatory cells in the myometrium were evaluated. The data indicate the absence of typical inflammatory reaction in the myometrium during elimination of smooth-muscle cells in the course of postpartum involution. Clasmatosis and apoptosis are hypothesized to be the main mechanisms providing reduction of the uterine weight after delivery.

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DNA in the rat uterus myometrium during pregnancy and postpartum involution

Cited by 25 publications

References 25 publications

Transforming growth factor-β 1 as a signal for induction of cell death by apoptosis

Transforming growth factor-β 1 as a signal for induction of cell death by apoptosis

Constitutive expression of calpain II in the rat uterus during pregnancy and involution

Structural Transformations of Myocytes during Gestation and Early Postpartum Involution of the Uterus

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