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Priyanka Parte - One of the best experts on this subject based on the ideXlab platform.
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Correction to: HDAC6 deacetylates alpha tubulin in sperm and modulates sperm motility in Holtzman Rat.
Cell and tissue research, 2017Co-Authors: Sweta Parab, Omshree Shetty, Reshma Gaonkar, Nafisa Balasinor, Vrinda Khole, Priyanka ParteAbstract:The published online version contains mistake. The chimeric peptide should read as 'DPSVLYVSLHRYGGYMNEGELRV'. It was inadvertently written as 'DPSVLYVSLYVSLHRYGGYMNEGELR' a mistake which we missed during proof reading.
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HDAC6 deacetylates alpha tubulin in sperm and modulates sperm motility in Holtzman Rat
Cell and Tissue Research, 2015Co-Authors: Sweta Parab, Omshree Shetty, Reshma Gaonkar, Nafisa Balasinor, Vrinda Khole, Priyanka ParteAbstract:Histone deacetylase 6 (HDAC6) is an alpha (α)-tubulin deacetylase and its over-expression has been demonstRated to promote chemotactic cell movement. Motility in sperm is driven by the flagella, the cytoskeletal structure comprising the microtubules, which are heterodimers of α- and β-tubulins. We have hypothesized that HDAC6, by virtue of being an α-tubulin deacetylase, might modulate sperm motility. However, the presence of HDAC6 on sperm has hitherto not been reported. In this study, we have demonstRated, for the first time, the presence of HDAC6 transcript and protein in the testicular and caudal sperm of Rat. We have observed a significantly overlapping expression of HDAC6 with acetyl α-tubulin (Ac α-tubulin) in the mid-piece and principal piece of sperm flagella, and the co-precipitation of α-tubulin and Ac α-tubulin together with HDAC6 and vice versa in sperm lysates. This indicates that HDAC6 interacts with α-tubulin. The HDAC6 activity of sperm, sperm motility and status of Ac α-tubulin investigated in the presence of HDAC inhibitors Trichostatin A, Tubastatin A and sodium butyRate demonstRate that HDAC6 in sperm is catalytically active and that inhibitors of HDAC6 increase acetylation and restrict sperm motility. Thus, we show that (1) active HDAC6 enzyme is present in sperm, (2) HDAC6 in sperm is able to deacetylate α-tubulin, (3) inhibition of HDAC6 results in increased Ac α-tubulin expression and (4) HDAC6 inhibition affects sperm motility. This evidence suggests that HDAC6 is involved in modulating sperm movement.
Sweta Parab - One of the best experts on this subject based on the ideXlab platform.
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Correction to: HDAC6 deacetylates alpha tubulin in sperm and modulates sperm motility in Holtzman Rat.
Cell and tissue research, 2017Co-Authors: Sweta Parab, Omshree Shetty, Reshma Gaonkar, Nafisa Balasinor, Vrinda Khole, Priyanka ParteAbstract:The published online version contains mistake. The chimeric peptide should read as 'DPSVLYVSLHRYGGYMNEGELRV'. It was inadvertently written as 'DPSVLYVSLYVSLHRYGGYMNEGELR' a mistake which we missed during proof reading.
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HDAC6 deacetylates alpha tubulin in sperm and modulates sperm motility in Holtzman Rat
Cell and Tissue Research, 2015Co-Authors: Sweta Parab, Omshree Shetty, Reshma Gaonkar, Nafisa Balasinor, Vrinda Khole, Priyanka ParteAbstract:Histone deacetylase 6 (HDAC6) is an alpha (α)-tubulin deacetylase and its over-expression has been demonstRated to promote chemotactic cell movement. Motility in sperm is driven by the flagella, the cytoskeletal structure comprising the microtubules, which are heterodimers of α- and β-tubulins. We have hypothesized that HDAC6, by virtue of being an α-tubulin deacetylase, might modulate sperm motility. However, the presence of HDAC6 on sperm has hitherto not been reported. In this study, we have demonstRated, for the first time, the presence of HDAC6 transcript and protein in the testicular and caudal sperm of Rat. We have observed a significantly overlapping expression of HDAC6 with acetyl α-tubulin (Ac α-tubulin) in the mid-piece and principal piece of sperm flagella, and the co-precipitation of α-tubulin and Ac α-tubulin together with HDAC6 and vice versa in sperm lysates. This indicates that HDAC6 interacts with α-tubulin. The HDAC6 activity of sperm, sperm motility and status of Ac α-tubulin investigated in the presence of HDAC inhibitors Trichostatin A, Tubastatin A and sodium butyRate demonstRate that HDAC6 in sperm is catalytically active and that inhibitors of HDAC6 increase acetylation and restrict sperm motility. Thus, we show that (1) active HDAC6 enzyme is present in sperm, (2) HDAC6 in sperm is able to deacetylate α-tubulin, (3) inhibition of HDAC6 results in increased Ac α-tubulin expression and (4) HDAC6 inhibition affects sperm motility. This evidence suggests that HDAC6 is involved in modulating sperm movement.
Richard E. Peterson - One of the best experts on this subject based on the ideXlab platform.
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2,3,7,8-Tetrachlorodibenzo-p-dioxin Inhibits Luminal Cell Differentiation and Androgen Responsiveness of the Ventral Prostate without Inhibiting Prostatic 5α-Dihydrotestosterone Formation or Testicular Androgen Production in Rat Offspring
Toxicological sciences : an official journal of the Society of Toxicology, 2000Co-Authors: H. Michael Theobald, Beth L. Roman, Tien-min Lin, Shintaro Ohtani, Shu-wen Chen, Richard E. PetersonAbstract:In utero and lactational exposure to a single maternal dose of 1 mg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg causes some overt toxicity and impairs prostate growth in male offspring. As similar effects on the ventral prostate can be caused by decreased testosterone production during perinatal development, we determined whether intRatesticular testosterone content, testicular responsiveness to go- nadotropin stimulation, or plasma testosterone concentRations were reduced in fetal and newborn Rats. Because these endpoints were not affected, the ability of TCDD exposure to inhibit synthesis of the proximal androgen in prostate development, 5a-dihydrotestosterone (DHT), from the circulating precursor testosterone and 5a-andro- stane-3a,17b-diol (3a-Diol), was studied on postnatal days (PNDs) 14, 21, and 32. The ability of the ventral prostate to form DHT from 3a-Diol was slightly impaired on PND 14, but this transient effect was not statistically significant, and recovery was evident by PND 21. Subsequent experiments used organ culture to study the effects of in vivo TCDD exposure on androgen metabolism, androgen responsive- ness, androgen receptor expression, and luminal epithelial cell differ- Exposure of male Holtzman Rat offspring in utero and via lactation to a single low dose of TCDD (0.064 -1.0 mg/kg maternal body weight) administered on GD 15 resulted in ventral prostate, epididymis, and seminal vesicle growth re- ductions (Mably et al., 1992a). In addition, in utero and lac- tational TCDD exposure decreased neonatal anogenital dis- tance, an external indicator of decreased androgenic status (Mably et al., 1992b), and reduced the responsiveness of the ventral prostate to androgenic growth stimulation in adulthood (Bjerke et al., 1994b). One possible explanation for these results is that in utero and lactational TCDD exposure reduces fetal plasma androgen concentRations. Indeed, our initial study in which male Holtzman Rat offspring were exposed to 1 mg TCDD/kg maternal body weight on GD 15 reported reduced plasma testosterone concentRations between GD's 17 and 21, and at 2 h after birth (Mably et al., 1992a). However, an independent study found no effect from GD 15 TCDD expo- sure on plasma testosterone concentRations in Long-Evans Rats on PND 0 (Gray et al., 1995). Another possible explanation for some of the seemingly antiandrogenic effects of TCDD, particularly with respect to prostate development, is that in utero and lactational exposure inhibits the formation of 5a-dihydrotestosterone (DHT). The Rat ventral prostate begins to arise before birth from the pros- tate anlagen in the urogenital sinus region. Prostatic mesen- chyme, under the influence of androgenic stimulation, induces the formation of epithelial buds that will eventually develop into secretory glands (Hayward et al., 1996). In order for this process to occur, however, circulating testosterone from the fetal testes must be enzymatically converted to DHT within the nascent prostate (George and Peterson, 1988). The develop- ment of the seminal vesicle and epididymis, like that of the prostate, requires androgenic stimulation. However, unlike the prostate, the seminal vesicle and epididymis do not require
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In utero and lactational exposure of the male Rat to 2,3,7,8-tetrachlorodibenzo-p-dioxin impairs prostate development. 2. Effects on growth and cytodifferentiation.
Toxicology and applied pharmacology, 1998Co-Authors: Beth L. Roman, Barry G. Timms, Gail S. Prins, Richard E. PetersonAbstract:Abstract In the male Holtzman Rat, in utero and lactational 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) exposure decreases prostate weight without inhibiting testicular androgen production or decreasing circulating androgen concentRations. Therefore, the present study sought to characterize effects of TCDD exposure on prostate development, from very early outgrowth from the urogenital sinus (Gestation Day [GD] 20) until rapid growth and differentiation are essentially complete (Postnatal Day [PND] 32). Pregnant Holtzman Rats were administered a single dose of TCDD (1.0 μg/kg po) or vehicle on GD 15 and offspring were exposed via placental transfer (GD 20 euthanasia) or placental and subsequent lactational transfer until euthanasia (if before PND 21) or weaning. Results show that the prostatic epithelial budding process was impaired by in utero TCDD exposure, as evidenced by significant decreases in the number of buds emerging from dorsal, lateral, and ventral aspects of the GD 20 urogenital sinus. Ventral prostate cell prolifeRation index was significantly decreased on PND 1 but was similar to or higher than control at later times, whereas apoptosis was an extremely rare event in ventral prostates from both control and TCDD-exposed animals. Delays were noted in the differentiation of pericordal smooth muscle cells and luminal epithelial cells. In addition, ventral prostates from approximately 40% of TCDD-exposed animals examined on PNDs 21 and 32 exhibited alteRations in the histological arrangement of cell types that could not be explained by a developmental delay. Compared to controls, these ventral prostates exhibited a disorganized, hyperplastic epithelium containing fewer luminal epithelial cells and an increased density or continuous layer of basal epithelial cells, as well as thicker periductal smooth muscle sheaths. In addition, in ventral prostates from TCDD-exposed animals, the intensity of androgen receptor staining was relatively low in the central and distal epithelium, and the number of androgen receptor-positive cells was relatively high in the periductal stroma. These data suggest that in utero and lactational TCDD exposure interferes with prostate development by decreasing very early epithelial growth, delaying cytodifferentiation, and, in the most severely affected animals, producing alteRations in epithelial and stromal cell histological arrangement and the spatial distribution of androgen receptor expression that may be of permanent consequence.
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Modulation of growth axis gene expression by in utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the weaning Holtzman Rat
Endocrine, 1996Co-Authors: Charles L. Chaffin, Richard E. Peterson, Rebecca S. Brogan, Reinhold J. Hutz, William B. WehrenbergAbstract:While the in utero and lactational effects of 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) on both male and female reproductive systems appear to be severe, little is known about its effects on the developing growth axis. The objective of this study was to describe changes in growth axis gene expression that accompany exposure to TCDD during in utero and lactational development. Pregnant Holtzman Rats were administered 1 μg TCDD/kg maternal body weight or vehicle control on gestational day 15 by gavage. Using ribonuclease protection assays, we compared mRNA levels measured in 21-d-old female pups exposed to TCDD with levels measured in control animals for the following genes: somatostatin, growth hormone-releasing hormone (GHRH), hypothalamic and pituitary galanin (GAL), growth hormone (GH), and insulin-like growth factor-I (IGF-I). Serum GH concentRations measured by radio-immunoassay were significantly increased, although GH mRNA levels were unchanged from controls by TCDD exposure. Hypothalamic GAL mRNA was decreased in TCDD-treated animals, whereas pituitary GAL mRNA in TCDD-treated animals was not altered. GHRH mRNA was increased in hypothalami from TCDD-exposed animals. IGF-I mRNA in the liver was decreased to 67% of controls. These data indicate that the growth axis is sensitive to the effects of TCDD delivered during critical periods of development. The alteRations observed in growth axis gene expression with exposure to TCDD add to the body of data demonstRating a potent effect of this compound on the fetal and neonatal endocrine system.
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In utero and lactational exposure of the male Holtzman Rat to 2,3,7,8-tetrachlorodibenzo-p-dioxin: decreased epididymal and ejaculated sperm numbers without alteRations in sperm transit Rate.
Toxicology and applied pharmacology, 1996Co-Authors: Rebecca J. Sommer, Danielle L. Ippolito, Richard E. PetersonAbstract:Decreased daily sperm production (DSP) and cauda epididymal sperm number (CESN) are some of the most sensitive effects of in utero and lactational 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure. The reduction in CESN cannot be fully accounted for by decreased spermatogenesis. To explain the decrease in CESN it was hypothesized that TCDD exposure increases the Rate of sperm transit through the excurrent duct system, thereby decreasing the number of sperm in the system at any given time. Pregnant Holtzman Rats were administered a single dose of TCDD (1.0 microgram/ kg,po) or vehicle on gestation day 15 and offspring were weaned on postnatal day (PND) 21. On PND 50, testicular sperm were labeled in five males per litter, from 30 control and 26 TCDD-exposed litters, by injecting 15 microCi [3H]thymidine into each testis, under general anesthesia. Sperm movement through the excurrent duct system was monitored daily 35-64 days post [3H]thymidine injection. On PNDs 92-93, TCDD exposure significantly decreased DSP/testis, corpus and cauda epididymis sperm numbers, vas deferens sperm number, and ejaculated sperm number by 28, 30, 36, 39, and 46%, respectively. The decreases in sperm number in the distal excurrent duct system were greater than the decrease in DSP, consistent with the hypothesis that TCDD exposure causes an effect other than decreased DSP that reduced epididymal and ejaculated sperm numbers. However, in utero and lactational TCDD exposure did not alter radiolabeled sperm transit time through the whole epididymis (15 days). With TCDD exposure causing no obvious alteRation in sperm transit Rate, a plausible explanation for the sperm loss is an increase in sperm phagocytosis in the excurrent duct system.
Vrinda Khole - One of the best experts on this subject based on the ideXlab platform.
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Correction to: HDAC6 deacetylates alpha tubulin in sperm and modulates sperm motility in Holtzman Rat.
Cell and tissue research, 2017Co-Authors: Sweta Parab, Omshree Shetty, Reshma Gaonkar, Nafisa Balasinor, Vrinda Khole, Priyanka ParteAbstract:The published online version contains mistake. The chimeric peptide should read as 'DPSVLYVSLHRYGGYMNEGELRV'. It was inadvertently written as 'DPSVLYVSLYVSLHRYGGYMNEGELR' a mistake which we missed during proof reading.
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HDAC6 deacetylates alpha tubulin in sperm and modulates sperm motility in Holtzman Rat
Cell and Tissue Research, 2015Co-Authors: Sweta Parab, Omshree Shetty, Reshma Gaonkar, Nafisa Balasinor, Vrinda Khole, Priyanka ParteAbstract:Histone deacetylase 6 (HDAC6) is an alpha (α)-tubulin deacetylase and its over-expression has been demonstRated to promote chemotactic cell movement. Motility in sperm is driven by the flagella, the cytoskeletal structure comprising the microtubules, which are heterodimers of α- and β-tubulins. We have hypothesized that HDAC6, by virtue of being an α-tubulin deacetylase, might modulate sperm motility. However, the presence of HDAC6 on sperm has hitherto not been reported. In this study, we have demonstRated, for the first time, the presence of HDAC6 transcript and protein in the testicular and caudal sperm of Rat. We have observed a significantly overlapping expression of HDAC6 with acetyl α-tubulin (Ac α-tubulin) in the mid-piece and principal piece of sperm flagella, and the co-precipitation of α-tubulin and Ac α-tubulin together with HDAC6 and vice versa in sperm lysates. This indicates that HDAC6 interacts with α-tubulin. The HDAC6 activity of sperm, sperm motility and status of Ac α-tubulin investigated in the presence of HDAC inhibitors Trichostatin A, Tubastatin A and sodium butyRate demonstRate that HDAC6 in sperm is catalytically active and that inhibitors of HDAC6 increase acetylation and restrict sperm motility. Thus, we show that (1) active HDAC6 enzyme is present in sperm, (2) HDAC6 in sperm is able to deacetylate α-tubulin, (3) inhibition of HDAC6 results in increased Ac α-tubulin expression and (4) HDAC6 inhibition affects sperm motility. This evidence suggests that HDAC6 is involved in modulating sperm movement.
Omshree Shetty - One of the best experts on this subject based on the ideXlab platform.
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Correction to: HDAC6 deacetylates alpha tubulin in sperm and modulates sperm motility in Holtzman Rat.
Cell and tissue research, 2017Co-Authors: Sweta Parab, Omshree Shetty, Reshma Gaonkar, Nafisa Balasinor, Vrinda Khole, Priyanka ParteAbstract:The published online version contains mistake. The chimeric peptide should read as 'DPSVLYVSLHRYGGYMNEGELRV'. It was inadvertently written as 'DPSVLYVSLYVSLHRYGGYMNEGELR' a mistake which we missed during proof reading.
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HDAC6 deacetylates alpha tubulin in sperm and modulates sperm motility in Holtzman Rat
Cell and Tissue Research, 2015Co-Authors: Sweta Parab, Omshree Shetty, Reshma Gaonkar, Nafisa Balasinor, Vrinda Khole, Priyanka ParteAbstract:Histone deacetylase 6 (HDAC6) is an alpha (α)-tubulin deacetylase and its over-expression has been demonstRated to promote chemotactic cell movement. Motility in sperm is driven by the flagella, the cytoskeletal structure comprising the microtubules, which are heterodimers of α- and β-tubulins. We have hypothesized that HDAC6, by virtue of being an α-tubulin deacetylase, might modulate sperm motility. However, the presence of HDAC6 on sperm has hitherto not been reported. In this study, we have demonstRated, for the first time, the presence of HDAC6 transcript and protein in the testicular and caudal sperm of Rat. We have observed a significantly overlapping expression of HDAC6 with acetyl α-tubulin (Ac α-tubulin) in the mid-piece and principal piece of sperm flagella, and the co-precipitation of α-tubulin and Ac α-tubulin together with HDAC6 and vice versa in sperm lysates. This indicates that HDAC6 interacts with α-tubulin. The HDAC6 activity of sperm, sperm motility and status of Ac α-tubulin investigated in the presence of HDAC inhibitors Trichostatin A, Tubastatin A and sodium butyRate demonstRate that HDAC6 in sperm is catalytically active and that inhibitors of HDAC6 increase acetylation and restrict sperm motility. Thus, we show that (1) active HDAC6 enzyme is present in sperm, (2) HDAC6 in sperm is able to deacetylate α-tubulin, (3) inhibition of HDAC6 results in increased Ac α-tubulin expression and (4) HDAC6 inhibition affects sperm motility. This evidence suggests that HDAC6 is involved in modulating sperm movement.