Hormonal regulation of programmed cell death during amphibian metamorphosis

1994 ◽  
Vol 72 (11-12) ◽  
pp. 581-588 ◽  
Author(s):  
Jamshed R. Tata
Keyword(s):  
Cell Death ◽  
Thyroid Hormone ◽  
Programmed Cell Death ◽  
Hormonal Regulation ◽  
Hormone Receptors ◽  
Amphibian Metamorphosis ◽  
Early Genes ◽  
Tadpole Tail ◽  
Inducible Genes ◽  
Promote Cell Death

Extensive programmed cell death (PCD) is initiated at the onset of amphibian metamorphosis, resulting in 100% of cells dying in some larval tissues, as during total regression of tail and gills. All cell death during metamorphosis is under the control of thyroid hormone (TH), which can initiate the process precociously in whole tadpoles or in individual tissues in culture. The hormone prolactin (PRL), given exogenously, prevents natural and TH-induced metamorphosis. We have exploited this dual hormonal regulation in premetamorphic Xenopus tails in organ culture to identify and characterize early genes that are TH-induced and considered important for initiating cell death. Among the earliest genes activated by TH are those encoding the two thyroid hormone receptors TRα and TRβ. This autoinduction of TR genes is considered important since, in blocking this process, PRL also inhibited the expression of other TH-inducible genes and prevented cell death. The expression of early genes other than TR genes, which are known to promote cell death or survival, is also considered to be important for the initiation of PCD during amphibian metamorphosis. We are, therefore, working on the identification, characterization, and expression of members of the Xenopus bcl-2-like gene family, as well as other genes, such as nur-77 and ICE, which may act as early genes during tadpole tail regression.Key words: cell death, thyroid hormones, Xenopus, metamorphosis, gene expression.

scholarly journals Elucidating the Neuroprotective Role of PPARs in Parkinson’s Disease: A Neoteric and Prospective Target

2021 ◽  
Vol 22 (18) ◽  
pp. 10161
Author(s):  
Tapan Behl ◽  
Piyush Madaan ◽  
Aayush Sehgal ◽  
Sukhbir Singh ◽  
Neelam Sharma ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Neurodegenerative Diseases ◽  
Hormone Receptors ◽  
Nerve Cells ◽  
Substantia Nigra Pars Compacta ◽  
Redox Equilibrium ◽  
Ppar Agonists

One of the utmost frequently emerging neurodegenerative diseases, Parkinson’s disease (PD) must be comprehended through the forfeit of dopamine (DA)-generating nerve cells in the substantia nigra pars compacta (SN-PC). The etiology and pathogenesis underlying the emergence of PD is still obscure. However, expanding corroboration encourages the involvement of genetic and environmental factors in the etiology of PD. The destruction of numerous cellular components, namely oxidative stress, ubiquitin-proteasome system (UPS) dysfunction, autophagy-lysosome system dysfunction, neuroinflammation and programmed cell death, and mitochondrial dysfunction partake in the pathogenesis of PD. Present-day pharmacotherapy can alleviate the manifestations, but no therapy has been demonstrated to cease disease progression. Peroxisome proliferator-activated receptors (PPARs) are ligand-directed transcription factors pertaining to the class of nuclear hormone receptors (NHR), and are implicated in the modulation of mitochondrial operation, inflammation, wound healing, redox equilibrium, and metabolism of blood sugar and lipids. Numerous PPAR agonists have been recognized to safeguard nerve cells from oxidative destruction, inflammation, and programmed cell death in PD and other neurodegenerative diseases. Additionally, various investigations suggest that regular administration of PPAR-activating non-steroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, indomethacin), and leukotriene receptor antagonists (montelukast) were related to the de-escalated evolution of neurodegenerative diseases. The present review elucidates the emerging evidence enlightening the neuroprotective outcomes of PPAR agonists in in vivo and in vitro models experiencing PD. Existing articles up to the present were procured through PubMed, MEDLINE, etc., utilizing specific keywords spotlighted in this review. Furthermore, the authors aim to provide insight into the neuroprotective actions of PPAR agonists by outlining the pharmacological mechanism. As a conclusion, PPAR agonists exhibit neuroprotection through modulating the expression of a group of genes implicated in cellular survival pathways, and may be a propitious target in the therapy of incapacitating neurodegenerative diseases like PD.

scholarly journals Thyroid Hormone Receptor β1 Expression in Developing Mouse Limbs and Face*

Endocrinology ◽  
1997 ◽  
Vol 138 (3) ◽  
pp. 1276-1281 ◽  
Author(s):  
Takeshi Nagasawa ◽  
Satoru Suzuki ◽  
Teiji Takeda ◽  
Leslie J. DeGroot
Keyword(s):  
Cerebral Cortex ◽  
Thyroid Hormone ◽  
Messenger Rna ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptor ◽  
Urogenital Sinus ◽  
Blue Staining ◽  
Functional Study ◽  
Fetal Life ◽  
Amphibian Metamorphosis

Abstract Thyroid hormone, acting through thyroid hormone receptors (TRs), plays an important role in amphibian metamorphosis and vertebrate development. To identify where and when TRβ1 promoter is activated during fetal life, we carried out an in vivo functional study of a 1.3 kilobase (kb) TRβ1 gene promoter using transgenic mice that express the β-galactosidase gene under control of the TRβ1 promoter. Transactivation of the gene was determined by blue staining of tissues after incubation with X-gal. High expression of transgene was detected in the limbs and face of the 12.5-day-old fetus (12.5F) and 14.5F, reminiscent of the changes occurring during amphibian metamorphosis, and this disappeared at 17.5F. The expression was confined to the tip of finger bones, between fingers in the limb buds, and was detected in the root of whisker follicles, nose, and around the eyes. Signal was detected in the oral cavity, nasal cavity, lung, and urogenital sinus of 14.5F, and disappeared at 17.5F. Signal was detected in the midbrain and auditory vesicles of 9.5F but was reduced between 12.5F and 17.5F, and there was no expression in the cerebral cortex layer of 0 days old neonates (P0). Expression was detected in the cortex after P5. There was signal in the cerebral cortex, cerebellum, kidney, and liver of adult mice. TRβ1 messenger RNA was detected by RT-PCR in the developing limbs and face. Transgene expression in the interdigital tissues, which regress during development, suggests that TRβ1 is expressed in mammals in areas undergoing apoptosis as well as in areas undergoing differentiation.

scholarly journals High Levels of Thyrotropin-Releasing Hormone Receptors Activate Programmed Cell Death in Human Pancreatic Precursors

Pancreas ◽  
2009 ◽  
Vol 38 (2) ◽  
pp. 197-202 ◽  
Author(s):  
Christopher M. Mulla ◽  
Elizabeth Geras-Raaka ◽  
Bruce M. Raaka ◽  
Marvin C. Gershengorn
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Hormone Receptors ◽  
Thyrotropin Releasing Hormone ◽  
Releasing Hormone

scholarly journals Hormonal regulation of the death commitment in programmed cell death of the silkworm anterior silk glands

2012 ◽  
Vol 58 (12) ◽  
pp. 1575-1581 ◽  
Author(s):  
Hiroto Matsui ◽  
Motonori Kakei ◽  
Masafumi Iwami ◽  
Sho Sakurai
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Hormonal Regulation ◽  
Silk Glands

scholarly journals Glucocorticoid and progesterone inhibit involution and programmed cell death in the mouse mammary gland.

1995 ◽  
Vol 131 (4) ◽  
pp. 1095-1103 ◽  
Author(s):  
Z Feng ◽  
A Marti ◽  
B Jehn ◽  
H J Altermatt ◽  
G Chicaiza ◽  
...  
Keyword(s):  
Cell Death ◽  
Mammary Gland ◽  
Programmed Cell Death ◽  
Hormone Receptors ◽  
Target Genes ◽  
Mouse Mammary Gland ◽  
Binding Activity ◽  
Steroid Hormone Receptors ◽  
Mrna Levels ◽  
Glucocorticoid Hormone

Milk production during lactation is a consequence of the suckling stimulus and the presence of glucocorticoids, prolactin, and insulin. After weaning the glucocorticoid hormone level drops, secretory mammary epithelial cells die by programmed cell death and the gland is prepared for a new pregnancy. We studied the role of steroid hormones and prolactin on the mammary gland structure, milk protein synthesis, and on programmed cell death. Slow-release plastic pellets containing individual hormones were implanted into a single mammary gland at lactation. At the same time the pups were removed and the consequences of the release of hormones were investigated histologically and biochemically. We found a local inhibition of involution in the vicinity of deoxycorticosterone- and progesterone-release pellets while prolactin-release pellets were ineffective. Dexamethasone, a very stable and potent glucocorticoid hormone analogue, inhibited involution and programmed cell death in all the mammary glands. It led to an accumulation of milk in the glands and was accompanied by an induction of protein kinase A, AP-1 DNA binding activity and elevated c-fos, junB, and junD mRNA levels. Several potential target genes of AP-1 such as stromelysin-1, c-jun, and SGP-2 that are induced during normal involution were strongly inhibited in dexamethasone-treated animals. Our results suggest that the cross-talk between steroid hormone receptors and AP-1 previously described in cells in culture leads to an impairment of AP-1 activity and to an inhibition of involution in the mammary gland implying that programmed cell death in the postlactational mammary gland depends on functional AP-1.

scholarly journals Apoptotic Machinery: The Bcl-2 Family Proteins in the Role of Inspectors and Superintendents

2006 ◽  
Vol 49 (1) ◽  
pp. 13-18 ◽  
Author(s):  
Aleš Tichý
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Manufacturing Process ◽  
Tissue Homeostasis ◽  
New Information ◽  
Key Players ◽  
Integral Role ◽  
Promote Cell Death ◽  
Death Signals

Programmed cell death, apoptosis, plays an integral role in a variety of biological events, e.g. morphogenesis, removal of unwanted or harmful cells, tissue homeostasis etc. Members of the Bcl-2 family have been described as the key players in the regulation of the apoptotic process. This family consists of proteins that prevent apoptosis (Bcl-2–like) and two structurally distinct subgroups (Bax-like and BH3–only) that on the contrary promote cell death. Majority of their response is concentrated to the mitochondrial level. In this paper, besides reviewing some new information in this field we focused on how they interact among each other and on the way they sense and influence the death signals from the environment. Here, we compare Bcl-2 family to inspectors and superintendents since they supervise the manufacturing process of cell death and they determine whether the cell will die or it will resist and survive.

scholarly journals Programmed cell death recruits macrophages into the developing mouse cochlea

2021 ◽  
Author(s):  
Vikrant Borse ◽  
Tejbeer Kaur ◽  
Ashley Hinton ◽  
Kevin Ohlemiller ◽  
Mark E. Warchol
Keyword(s):  
Cell Death ◽  
Thyroid Hormone ◽  
Programmed Cell Death ◽  
Critical Role ◽  
Large Population ◽  
Developmental Time ◽  
Macrophage Recruitment ◽  
Time Period ◽  
Developmental Cell Death

AbstractProgrammed cell death (PCD) plays a critical role in the development and maturation of the cochlea. Significant remodeling occurs among cells of the greater epithelial ridge (GER) of Kölliker’s organ, leading to tissue regression and formation of the inner sulcus. In mice, this event normally occurs between postnatal days 5-15 (P5-15) and is regulated by thyroid hormone (T3). During this developmental time period, the cochlea also contains a large population of macrophages. Macrophages are frequently involved in the phagocytic clearance of dead cells, both during development and after injury, but the role of macrophages in the developing cochlea is unknown. This study examined the link between developmental cell death in the GER and the recruitment of macrophages into this region. Cell death in the basal GER begins at P5 and enhanced numbers of macrophages were observed at P7. This pattern of macrophage recruitment was unchanged in mice that were genetically deficient for CX3CR1, the receptor for fractalkine (a known macrophage chemoattractant). We found that injection of T3 at P0 and P1 caused GER cell death to begin at P3, and this premature PCD was accompanied by earlier recruitment of macrophages. We further found that depletion of macrophages from the developing cochlea (using CX3CR1DTR/+ mice and treatment with the CSF1R antagonist BLZ945) had no effects on the pattern of GER regression. Together, these findings suggest that macrophages are recruited into the GER region after initiation of developmental PCD, but that they are not essential for GER regression during cochlear remodeling.

Programmed cell death during amphibian metamorphosis

2005 ◽  
Vol 16 (2) ◽  
pp. 271-280 ◽  
Author(s):  
Keisuke Nakajima ◽  
Kenta Fujimoto ◽  
Yoshio Yaoita
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Amphibian Metamorphosis

scholarly journals Developmental expression and hormonal regulation of glucocorticoid and thyroid hormone receptors during metamorphosis in Xenopus laevis

2004 ◽  
Vol 181 (1) ◽  
pp. 91-104 ◽  
Author(s):  
LP Krain ◽  
RJ Denver
Keyword(s):  
Thyroid Hormone ◽  
Xenopus Laevis ◽  
Hormone Receptor ◽  
Hormone Receptors ◽  
Mrna Level ◽  
Stress Hormones ◽  
Receptor Expression ◽  
Developmental Expression ◽  
Amphibian Metamorphosis ◽  
The Brain

Corticosteroids, the primary circulating vertebrate stress hormones, are known to potentiate the actions of thyroid hormone in amphibian metamorphosis. Environmental modulation of the production of stress hormones may be one way that tadpoles respond to variation in their larval habitat, and thus control the timing of metamorphosis. Thyroid hormone and corticosteroids act through structurally similar nuclear receptors, and interactions at the transcriptional level could lead to regulation of common pathways controlling metamorphosis. To better understand the roles of corticosteroids in amphibian metamorphosis we analyzed the developmental and hormone-dependent expression of glucocorticoid receptor (GR) mRNA in the brain (diencephalon), intestine and tail of Xenopus laevis tadpoles. We compared the expression patterns of GR with expression of thyroid hormone receptor beta (TRbeta). In an effort to determine the relationship between nuclear hormone receptor expression and levels of ligand, we also analyzed changes in whole-body content of 3,5,3'-triiodothyronine (T(3)), thyroxine, and corticosterone (CORT). GR transcripts of 8, 4 and 2 kb were detected in all tadpole tissues, but only the 4 and 2 kb transcripts could be detected in embryos. The level of GR mRNA was low during premetamorphosis in the brain but increased significantly during prometamorphosis, remained at a constant level throughout metamorphosis, and increased to its highest level in the juvenile frog. GR mRNA level in the intestine remained relatively constant, but increased in the tail throughout metamorphosis, reaching a maximum at metamorphic climax. The level of GR mRNA was increased by treatment with CORT in the intestine but not in the brain or tail. TRbeta mRNA level increased in the brain, intestine and tail during metamorphosis and was induced by treatment with T(3). Analysis of possible crossregulatory relationships between GRs and TRs showed that GR mRNA was upregulated by exogenous T(3) (50 nM) in the tail but downregulated in the brain of premetamorphic tadpoles. Exogenous CORT (100 nM) upregulated TRbeta mRNA in the intestine. Our findings provide evidence for tissue-specific positive, negative and crossregulation of nuclear hormone receptors during metamorphosis of X. laevis. The synergy of CORT with T(3) on tadpole tail resorption may depend on the accelerated accumulation of GR transcripts in this tissue during metamorphosis, which may be driven by rising plasma thyroid hormone titers.

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