Browsing by Author "Tatar, M."

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Altered luteal expression patterns of genomic and non-genomic progesterone receptors in bitches at different reproductive states
(2024) Ucar, E.H.; Peker, C.; Hitit, M.; Kose, M.; Tatar, M.; Bozkaya, F.; Atli, M.O.
The binding of steroid hormones to their specific receptors is necessary to exert their effects on target cells. Progesterone (P), a steroid hormone, carries out its effects through both genomic and non-genomic (the cell membrane-associated) receptors. This study aimed to ascertain luteal expression patterns of genomic and non-genomic progesterone receptors in bitches in physiological (early dioestrus and early pregnant) and pathological (pyometra) reproductive states. Luteal tissue was collected from the bitches at early dioestrus (ED, n = 5), early pregnant (EP, n = 5), and pyometra (PY, n = 5). The expression profiles of Steroidogenic Acute Regulator Protein (STAR), Progesterone Receptor (PGR), Membrane Progestin Receptors (PAQR5, PAQR7 and PAQR8), and Progesterone Membrane Components (PGMRC1 and PGMRC2) were examined at the mRNA levels using Real-Time Polymerase Chain Reaction (RT-PCR). Protein levels of PGR, PGMRC1 and PGMRC2 were detected by western blotting (WB). The STAR expression was found in all groups, with a statistical difference observed between EP and PY groups (P < 0.05). The protein level of PGR was determined to be highest in the EP group and lowest in the PY group. The expression of PAQR8 increased in the EP group (P < 0.05). The PAQR5 exhibited high expression in the EP group and low expression in the PY group (P < 0.05). PGRMC1 was more elevated in the EP group and lower in the PY group (P < 0.05). Protein levels of PGMRC1 and PGMRC2 were also observed at the highest expression in EP group. According to the altered expression profiles for examined receptors, we suggest that those progesterone receptors have roles in early pregnancy or pyometra in bitches.
Altered luteal expression patterns of genomic and non-genomic progesterone receptors in bitches at different reproductive states
(2024.01.01) Ucar, E.H.; Peker, C.; Hitit, M.; Kose, M.; Tatar, M.; Bozkaya, F.; Atli, M.O.
The binding of steroid hormones to their specific receptors is necessary to exert their effects on target cells. Progesterone (P-4), a steroid hormone, carries out its effects through both genomic and non-genomic (the cell membrane-associated) receptors. This study aimed to ascertain luteal expression patterns of genomic and non-genomic progesterone receptors in bitches in physiological (early dioestrus and early pregnant) and pathological (pyometra) reproductive states. Luteal tissue was collected from the bitches at early dioestrus (ED, n = 5), early pregnant (EP, n = 5), and pyometra (PY, n = 5). The expression profiles of Steroidogenic Acute Regulator Protein (STAR), Progesterone Receptor (PGR), Membrane Progestin Receptors (PAQR5, PAQR7 and PAQR8), and Progesterone Membrane Components (PGMRC1 and PGMRC2) were examined at the mRNA levels using Real-Time Polymerase Chain Reaction (RT-PCR). Protein levels of PGR, PGMRC1 and PGMRC2 were detected by western blotting (WB). The STAR expression was found in all groups, with a statistical difference observed between EP and PY groups (P < 0.05). The protein level of PGR was determined to be highest in the EP group and lowest in the PY group. The expression of PAQR8 increased in the EP group (P < 0.05). The PAQR5 exhibited high expression in the EP group and low expression in the PY group (P < 0.05). PGRMC1 was more elevated in the EP group and lower in the PY group (P < 0.05). Protein levels of PGMRC1 and PGMRC2 were also observed at the highest expression in EP group. According to the altered expression profiles for examined receptors, we suggest that those progesterone receptors have roles in early pregnancy or pyometra in bitches.
Altered luteal expression patterns of genomic and non-genomic progesterone receptors in bitches at different reproductive states
(Elsevier Inc., 2024) Ucar, E.H.; Peker, C.; Hitit, M.; Kose, M.; Tatar, M.; Bozkaya, F.; Atli, M.O.
The binding of steroid hormones to their specific receptors is necessary to exert their effects on target cells. Progesterone (P4), a steroid hormone, carries out its effects through both genomic and non-genomic (the cell membrane-associated) receptors. This study aimed to ascertain luteal expression patterns of genomic and non-genomic progesterone receptors in bitches in physiological (early dioestrus and early pregnant) and pathological (pyometra) reproductive states. Luteal tissue was collected from the bitches at early dioestrus (ED, n = 5), early pregnant (EP, n = 5), and pyometra (PY, n = 5). The expression profiles of Steroidogenic Acute Regulator Protein (STAR), Progesterone Receptor (PGR), Membrane Progestin Receptors (PAQR5, PAQR7 and PAQR8), and Progesterone Membrane Components (PGMRC1 and PGMRC2) were examined at the mRNA levels using Real-Time Polymerase Chain Reaction (RT-PCR). Protein levels of PGR, PGMRC1 and PGMRC2 were detected by western blotting (WB). The STAR expression was found in all groups, with a statistical difference observed between EP and PY groups (P < 0.05). The protein level of PGR was determined to be highest in the EP group and lowest in the PY group. The expression of PAQR8 increased in the EP group (P < 0.05). The PAQR5 exhibited high expression in the EP group and low expression in the PY group (P < 0.05). PGRMC1 was more elevated in the EP group and lower in the PY group (P < 0.05). Protein levels of PGMRC1 and PGMRC2 were also observed at the highest expression in EP group. According to the altered expression profiles for examined receptors, we suggest that those progesterone receptors have roles in early pregnancy or pyometra in bitches.
An investigation of the distributions of ferroptosis and necroptosis mediators in the maternal-fetal interface at different days of rat pregnancy
(2023) Tatar, M.; Tüfekci, K. K.
Ferroptosis and necroptosis are recognized as playing major roles in the regulation of various physiological processes. However, the physiological role of the cell death mediated by these two pathways in the developmental process has not yet been clearly established. This study investigated ferroptosis and necroptosis signalling pathways in maternal-fetal tissue in the different gestational days (GD) of rat pregnancy using immunohistochemical and western blot methods in order to fill this gap. Twenty-four female Wistar albino rats were mated and divided into three groups. Maternal-fetal tissue samples were collected on GD 5, 12 and 19 of pregnancy. Expression and total protein levels of the markers glutathione peroxidase-4, soluble transporter family 7 member 11, transferrin receptor, receptor-interacting serine/threonine-protein kinase 1, receptor-interacting serine/threonine-protein kinase 3 and mixed lineage kinase domain-like protein were investigated on both the maternal and fetal surfaces of the placenta using immunohistochemical and western blot methods. The results showed varying levels of protein expression of both ferroptosis and necroptosis mediators in the GD 5, 12 and 19 of pregnancy. Immunohistochemical analyses revealed that these mediators were located on both the maternal (decidua and metrial gland) and fetal surfaces (labyrinth zone, yolk sac and basal zone) and that their expression levels changed in the different GD. The findings revealed the existence of important ferroptosis and necroptosis pathway mediators in rat maternal-fetal tissue. These results may provide a molecular framework for a better understanding of the communication between the placenta, decidua and fetus during the developmental process.
An investigation of the distributions of ferroptosis and necroptosis mediators in the maternal–fetal interface at different days of rat pregnancy
(John Wiley and Sons Inc, 2024) Tatar, M.; Tüfekci, K.K.
Ferroptosis and necroptosis are recognized as playing major roles in the regulation of various physiological processes. However, the physiological role of the cell death mediated by these two pathways in the developmental process has not yet been clearly established. This study investigated ferroptosis and necroptosis signalling pathways in maternal–fetal tissue in the different gestational days (GD) of rat pregnancy using immunohistochemical and western blot methods in order to fill this gap. Twenty-four female Wistar albino rats were mated and divided into three groups. Maternal–fetal tissue samples were collected on GD 5, 12 and 19 of pregnancy. Expression and total protein levels of the markers glutathione peroxidase-4, soluble transporter family 7 member 11, transferrin receptor, receptor-interacting serine/threonine-protein kinase 1, receptor-interacting serine/threonine-protein kinase 3 and mixed lineage kinase domain-like protein were investigated on both the maternal and fetal surfaces of the placenta using immunohistochemical and western blot methods. The results showed varying levels of protein expression of both ferroptosis and necroptosis mediators in the GD 5, 12 and 19 of pregnancy. Immunohistochemical analyses revealed that these mediators were located on both the maternal (decidua and metrial gland) and fetal surfaces (labyrinth zone, yolk sac and basal zone) and that their expression levels changed in the different GD. The findings revealed the existence of important ferroptosis and necroptosis pathway mediators in rat maternal–fetal tissue. These results may provide a molecular framework for a better understanding of the communication between the placenta, decidua and fetus during the developmental process.
An investigation of the distributions of ferroptosis and necroptosis mediators in the maternal-fetal interface at different days of rat pregnancy
(2023.01.01) Tatar, M.; Tüfekci, K.K.
Ferroptosis and necroptosis are recognized as playing major roles in the regulation of various physiological processes. However, the physiological role of the cell death mediated by these two pathways in the developmental process has not yet been clearly established. This study investigated ferroptosis and necroptosis signalling pathways in maternal-fetal tissue in the different gestational days (GD) of rat pregnancy using immunohistochemical and western blot methods in order to fill this gap. Twenty-four female Wistar albino rats were mated and divided into three groups. Maternal-fetal tissue samples were collected on GD 5, 12 and 19 of pregnancy. Expression and total protein levels of the markers glutathione peroxidase-4, soluble transporter family 7 member 11, transferrin receptor, receptor-interacting serine/threonine-protein kinase 1, receptor-interacting serine/threonine-protein kinase 3 and mixed lineage kinase domain-like protein were investigated on both the maternal and fetal surfaces of the placenta using immunohistochemical and western blot methods. The results showed varying levels of protein expression of both ferroptosis and necroptosis mediators in the GD 5, 12 and 19 of pregnancy. Immunohistochemical analyses revealed that these mediators were located on both the maternal (decidua and metrial gland) and fetal surfaces (labyrinth zone, yolk sac and basal zone) and that their expression levels changed in the different GD. The findings revealed the existence of important ferroptosis and necroptosis pathway mediators in rat maternal-fetal tissue. These results may provide a molecular framework for a better understanding of the communication between the placenta, decidua and fetus during the developmental process.
An investigation of the endoplasmic reticulum stress in obesity exposure in the prenatal period
(2023.01.01) Tüfekci, K.K.; Tatar, M.; Terzi, F.; Bakirhan, E.G.
Objectives: Exposure to maternal obesity has been shown to make offspring more prone to cognitive and metabolic disorders later in life. Although the underlying mechanisms are unclear, the role of endoplasmic reticulum (ER) stress in the fetal programming process is remarkable. ER stress can be activated by many chronic diseases, including obesity and diabetes. Therefore, our study aimed to investigate the role of ER stress caused by maternal diet-induced obesity in the offspring hippocampus. We also evaluated the protective effect of N-acetylcysteine (NAC) against ER stress.Methods: A rat obesity model was created by providing a high-fat (60 % kcal) diet. N-acetylcysteine (NAC) was administered at a dosage of 150 mg/kg via the intragastric route. The animals were mated at the age of 12 weeks. The same diet was maintained during pregnancy and lactation. The experiment was terminated on the postnatal 28th day, and the offspring's brain tissues were examined. Immunohistochemical staining for ER stress markers was performed on sections taken from tissues after routine histological procedures.Results: The results revealed increased GRP78, PERK, and eIF2 alpha immunoreactivities in the hippocampal dentate gyrus (DG) and cornu ammonis 1 (CA1) regions in the obese group offspring, while the expression of those markers in those regions normalized with NAC supplementation (p < 0.01). Statistical analysis of XBP1 immunoreactivity H-scores revealed no difference between the study groups (p > 0.05).Discussion: These results suggest that exposure to obesity during the prenatal period may cause increased ER stress in hippocampal neurons, which have an important role in the regulation of learning, memory and behavior, and this may contribute to decreased cognitive performance. On the other hand, NAC stands out as an effective agent that can counteract hippocampal ER stress.
An investigation of the endoplasmic reticulum stress in obesity exposure in the prenatal period
(Elsevier, 2023) Tüfekci, K.K.; Tatar, M.; Terzi, F.; Bakirhan, E. G.
Objectives: Exposure to maternal obesity has been shown to make offspring more prone to cognitive and metabolic disorders later in life. Although the underlying mechanisms are unclear, the role of endoplasmic reticulum (ER) stress in the fetal programming process is remarkable. ER stress can be activated by many chronic diseases, including obesity and diabetes. Therefore, our study aimed to investigate the role of ER stress caused by maternal diet-induced obesity in the offspring hippocampus. We also evaluated the protective effect of N-acetylcysteine (NAC) against ER stress. Methods: A rat obesity model was created by providing a high-fat (60% kcal) diet. Nacetylcysteine (NAC) was administered at a dosage of 150 mg/kg via the intragastric route. The animals were mated at the age of 12 weeks. The same diet was maintained during pregnancy and lactation. The experiment was terminated on the postnatal 28th day, and the offspring's brain tissues were examined. Immunohistochemical staining for ER stress markers was performed on sections taken from tissues after routine histological procedures. Results: The results revealed increased GRP78, PERK, and eIF2α immunoreactivities in the hippocampal dentate gyrus (DG) and cornu ammonis 1 (CA1) regions in the obese group offspring, while the expression of those markers in those regions normalized with NAC supplementation (p<0.01). Statistical analysis of XBP1 immunoreactivity H-scores revealed no difference between the study groups (p>0.05). Discussion: These results suggest that exposure to obesity during the prenatal period may cause increased ER stress in hippocampal neurons, which have an important role in the regulation of learning, memory and behavior, and this may contribute to decreased cognitive performance. On the other hand, NAC stands out as an effective agent that can counteract hippocampal ER stress.
Endoplasmic reticulum stress and associated apoptosis are linked with the pathogenesis of white striping in broiler breast muscles
(2024) İpek, E.; Ahsan, U.; Özsoy, B.; Aşıcı, G.S.E.; Tatar, M.; Özpilavcı, B.N.; Epikmen, E.T.; Özsoy, Ş.Y.; Khamseh, E.K.; Petracci, M.
White striping (WS) that appears as white stripes parallel to the muscle fibrils is an emerging growth-related abnormality of broiler breast meat. The pathomechanism of this defect has not been fully understood despite intensive studies over the past decade. In the present study, endoplasmic reticulum (ER) stress and its associated apoptotic pathways were investigated to elucidate the potential role of these pathways in the development of WS. To this end, a total of 60 Pectoralis major (Pm) muscle samples were collected from 55-d-old Ross 308 male broiler chickens according to the severity of gross WS lesions (normal, mild, and severe). Histopathological and molecular analyses were conducted to evaluate the lesions and genes involved in the ER stress and related apoptosis. All the Pm samples, both with and without macroscopic WS lesions, showed varying degrees of myodegenerative lesions. Molecular analysis revealed that the transcript abundances of many components related to protein kinase R-like ER kinase (PERK) and inositol-requiring enzyme type 1 (IRE-1) signals of the ER stress response were significantly greater in severely WS-affected breast tissues compared to their mildly affected and normal counterparts. Similarly, the transcript abundances of apoptotic markers related to both signaling pathways were significantly greater in severe WS lesions than those of mildly affected and normal Pm tissues. Besides these, a significant increase in caspase-3 transcript abundance was seen in severe WS lesions in comparison with mild WS and normal breast muscles. Findings of this study suggest that ER stress response and its related apoptotic pathways are possibly activated in the breast muscle of broiler chickens with severe WS lesions. Based on these findings, it is speculated that ER stress-mediated apoptosis occupies a central role in the progression of WS in broiler chickens.
Endoplasmic reticulum stress and associated apoptosis are linked with the pathogenesis of white striping in broiler breast muscles
(Elsevier Inc., 2024) İpek, E.; Ahsan, U.; Özsoy, B.; Ekren Aşıcı, G.S.; Tatar, M.; Özpilavcı, B.N.; Epikmen, E.T.; Özsoy, Ş.Y.; Khamseh, E.K.; Petracci, M.
White striping (WS) that appears as white stripes parallel to the muscle fibrils is an emerging growth-related abnormality of broiler breast meat. The pathomechanism of this defect has not been fully understood despite intensive studies over the past decade. In the present study, endoplasmic reticulum (ER) stress and its associated apoptotic pathways were investigated to elucidate the potential role of these pathways in the development of WS. To this end, a total of 60 Pectoralis major (Pm) muscle samples were collected from 55-d-old Ross 308 male broiler chickens according to the severity of gross WS lesions (normal, mild, and severe). Histopathological and molecular analyses were conducted to evaluate the lesions and genes involved in the ER stress and related apoptosis. All the Pm samples, both with and without macroscopic WS lesions, showed varying degrees of myodegenerative lesions. Molecular analysis revealed that the transcript abundances of many components related to protein kinase R-like ER kinase (PERK) and inositol-requiring enzyme type 1 (IRE-1) signals of the ER stress response were significantly greater in severely WS-affected breast tissues compared to their mildly affected and normal counterparts. Similarly, the transcript abundances of apoptotic markers related to both signaling pathways were significantly greater in severe WS lesions than those of mildly affected and normal Pm tissues. Besides these, a significant increase in caspase-3 transcript abundance was seen in severe WS lesions in comparison with mild WS and normal breast muscles. Findings of this study suggest that ER stress response and its related apoptotic pathways are possibly activated in the breast muscle of broiler chickens with severe WS lesions. Based on these findings, it is speculated that ER stress-mediated apoptosis occupies a central role in the progression of WS in broiler chickens.
Expression and distribution of GPR55 and GPR119 during the development of rat testis
(2023.01.01) Tutun, H.; Ipek, V.; Tatar, M.; Kizilyer, A.; Kaya, M.M.
G Protein-Coupled Receptors, GPR55 and GPR119 are widely distributed throughout the body and exert important biological functions. However, little is known about their roles in testis. This study aimed to examine the expression and distribution of GPR55 and GPR119 during the development of the rat testis. Sixty male Sprague Dawley rats (180-240 g) were divided into 10 groups as 7, 14, 21, 28, 35, 42, 49, 56, 63, and 70 postnatal days of age (PND) (six animals per group). The testicular expression of GPR55 and GPR119 has been investigated by immunohistochemistry, Western blot, and quantitative RT-PCR methods. We observed that GPR55 and GPR119 are expressed throughout the rat testis development from PND 7 to 70. However, no difference was observed between the groups in terms of expression levels, except for GPR55 mRNA expression in the group of PND 7. Immunohistochemistry analysis showed that GPR55 is expressed in spermatids and spermatocytes in the mid-term tubules and spermatocytes in the late-stage tubules in groups of PND 56, 63, and 70. For GPR119, very intense positivity was observed only in spermatids in the mid-term (stage VII-VIII) tubules in the groups of PND 56, 63, and 70. No significant difference was observed in the number of GPR55 and GPR119 positive cells in testes from PND 56 through PND 70. Taken together, both GPR55 and GPR119 receptors are expressed throughout the rat testis development (PND 7 to 70). These results suggest that GPR55 and GPR119 are involved in the modulation of male reproductive function.
Oleuropein Mitigates Acrylamide-Induced Nephrotoxicity by Affecting Placental Growth Factor Immunoactivity in the Rat Kidney
(2023-10) Tüfekci, K.K.; Tatar, M.
The liver is susceptible to toxic effects, as it is the main site of acrylamide biotransformation and detoxification. Researchers have claimed that placental growth factor (PlGF) and its pathway are potentially involved in numerous diseases, including liver fibrosis and angiogenesis. Oleuropein is a natural phenolic compound with potent antioxidant effects. The purpose of this study was to examine the role of PlGF and the potential protection provided by oleuropein in acrylamide hepatotoxicity. Wistar albino rats were assigned into control, acrylamide (ACR) (5 mg/kg), oleuropein (OLE) (4.2 mg/kg), and ACR+OLE groups. Acrylamide and oleuropein were administered for 21 days. The control group received only physiological saline. Liver tissues were evaluated histologically and immunohistochemically. Histological examinations revealed significant enlargement of the sinusoidal vessels and abundant hepatocytes with pyknotic nuclei in the ACR group. Acrylamide toxicity resulted in elevated PlGF, accumulation of 8-hydroxydeoxyguanosine (8-OHdG), and increased Caspase-3 immunoreactivity in the liver. Oleuropein treatment reduced the increased expression of PlGF, 8-OHdG, and Caspase-3 against these deleterious effects observed in the ACR group. A positive correlation was observed between PlGF levels as well as oxidative stress and apoptosis markers in acrylamide toxicity. Oleuropein probably counteracted this mechanism by exhibiting antioxidant activity.
Oleuropein Mitigates Acrylamide-Induced Nephrotoxicity by Affecting Placental Growth Factor Immunoactivity in the Rat Kidney
(2023.01.01) Tüfekci, K.K.; Tatar, M.
Objective: Oleuropein is one of the main components of the antioxidant properties of olive leaves. Placental growth factor is an important regulator in angiogenesis and inflammation, its levels being variable in pathological conditions. In this study, we aimed to examine changes in placental growth factor expression and the effect of oleuropein, found in olive leaves, in rats exposed to acrylamide nephrotoxicity. Material and Methods: Twenty-four male Wistar albino rats were allocated into 4 groups. The control group received saline solution only. The oleuropein group received oleuropein (4.2 mg/kg), the acrylamide group received acrylamide (5 mg/kg), and the acrylamide and oleuropein group received acrylamide (5 mg/kg) and oleuropein (4.2 mg/kg). All substances were administered via gastric gavage for 21 days. Kidney tissues were removed at the end of the study and subjected to histopathological, stereological, and immunohistochemical procedures. Results: Histopathological examination revealed dilatation, vacuolization, and degeneration in the proximal and distal tubules and increased placental growth factor immunoreactivity in the acrylamide group. Cavalieri volume analysis revealed increased cortex, distal, and proximal tubule volumes (P < .01). Conclusion: Oleuropein significantly attenuated acrylamide-induced kidney injury by altering placental growth factor immunoreactivity. Placental growth factor immunoreactivity can be used as a marker of acryl-amide nephrotoxicity, and oleuropein may counteract acrylamide-induced kidney injury.
Protective Effect of Myricetin Against Experimentally Induced Torsion in Rats
(2023.01.01) Tatar, M.; Polat, Z.; Öner, J.; Öner, H.
Testicular torsion causes ischemia and free radical formation by obstructing vascular flow caused by complete or partial rotation of the testis. Myricetin is a plant-derived flavonoid with various biological effects, such as potent anti-oxidation and anti-inflammatory properties. The study aims to evaluate the protective effects of myricetin on the apoptosis of testicular germ cells after experimental testicular torsion. Twenty-four Wistar albino rats were divided into four groups; Control, Sham, Torsion group (720 deg torsion for 2 h), and Myricetin group (torsion model was created, and myricetin injection (1.5 mg/kg) was done during seven days). End of the experiment, testis tissues were removed and fixed in Bouin's solution. Crossman's triple stain was done to determine the histological changes. Also, 8-OHdG and Caspase-3 immunoreactivities were assessed, and TUNEL staining was done. According to the results, we found that 8-OHdG, Caspase-3 immunoreactivity, and TUNEL-positive cells increased, accompanied by several histopathological changes in the torsion group. In contrast, myricetin significantly attenuated testicular injury by reducing apoptosis and DNA damage. These findings suggest that myricetin protects testes against torsion-induced damage in rats, possibly by reducing oxidative stress and inhibiting apoptosis. Our study provides a theoretical basis for further research into maintaining male reproductive health.