@article{MTMT:34763013,
	title = {Stress-Induced Changes in Nucleocytoplasmic Localization of Crucial Factors in Gene Expression Regulation},
	url = {https://m2.mtmt.hu/api/publication/34763013},
	author = {Khamit, Ali and Chakraborty, Payal and Zahorán, Szabolcs and Villanyi, Zoltan and Orvos, Hajnalka and Hermesz, Edit},
	doi = {10.3390/ijms25073895},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {25},
	unique-id = {34763013},
	issn = {1661-6596},
	abstract = {This study investigates the toxic effect of harmful materials, unfiltered by the placenta, on neonatal umbilical cord (UC) vessels, focusing on stress-induced adaptations in transcriptional and translational processes. It aims to analyze changes in pathways related to mRNA condensate formation, transcriptional regulation, and DNA damage response under maternal smoking-induced stress. UC vessels from neonates born to smoking (Sm) and nonsmoking mothers (Ctr) were examined. Immunofluorescence staining and confocal microscopy assessed the localization of key markers, including Transcription Complex Subunit 1 (CNOT1) and the largest subunit of RNA polymerase II enzyme (RPB1). Additionally, markers of DNA damage response, such as Poly(ADP-ribose) polymerase-1, were evaluated. In Sm samples, dissolution of CNOT1 granules in UC vessels was observed, potentially aiding stalled translation and enhancing transcription via RPB1 assembly and translocation. Control vessels showed predominant cytoplasmic RPB1 localization. Despite adaptive responses, Sm endothelial cells exhibited significant damage, indicated by markers like Poly(ADP-ribose) polymerase-1. Ex vivo metal treatment on control vessels mirrored Sm sample alterations, emphasizing marker roles in cell survival under toxic exposure. Maternal smoking induces specific molecular adaptations in UC vessels, affecting mRNA condensate formation, transcriptional regulation, and DNA damage response pathways. Understanding these intricate molecular mechanisms could inform interventions to improve neonatal health outcomes and mitigate adverse effects of toxic exposure during pregnancy.},
	year = {2024},
	eissn = {1422-0067},
	orcid-numbers = {Khamit, Ali/0000-0002-5405-7702; Zahorán, Szabolcs/0000-0002-6649-8249; Orvos, Hajnalka/0000-0001-9400-865X; Hermesz, Edit/0000-0002-0543-6693}
}

@article{MTMT:34070326,
	title = {Molecular Study on Twin Cohort with Discordant Birth Weight},
	url = {https://m2.mtmt.hu/api/publication/34070326},
	author = {Chakraborty, Payal and Orvos, Hajnalka and Hermesz, Edit},
	doi = {10.3390/antiox12071370},
	journal-iso = {ANTIOXIDANTS-BASEL},
	journal = {ANTIOXIDANTS},
	volume = {12},
	unique-id = {34070326},
	abstract = {The increased rate of twinning has pointed out newer challenges in clinical practices related to gestational complications, intrauterine growth restriction, perinatal mortality, and comorbidities. As a twin pregnancy progresses, the increased demand for oxygen supply can easily disrupt the redox homeostasis balance and further impose a greater challenge for the developing fetuses. A substantial birth-weight difference acts as an indicator of a deficit in oxygenation or blood flow to one of the fetuses, which might be related to a low bioavailable nitric oxide level. Therefore, in this study, we focused on networks involved in the adjustment of oxygen supply, like the activation of inducible and endothelial nitric oxide synthase (NOS3) along with free radical and lipid peroxide formation in mature twin pairs with high birth-weight differences. The selected parameters were followed by immunofluorescence staining, fluorescence-activated cell sorting analysis, and biochemical measurements in the umbilical cord vessels and fetal red blood cells. Based on our data set, it is clear that the lower-weight siblings are markedly exposed to persistent intrauterine hypoxic conditions, which are connected to a decreased level in NOS3 activation. Furthermore, the increased level of peroxynitrite aggravates lipid peroxidation and induces morphological and functional damage and loss in redox homeostasis.},
	year = {2023},
	eissn = {2076-3921},
	orcid-numbers = {Orvos, Hajnalka/0000-0001-9400-865X; Hermesz, Edit/0000-0002-0543-6693}
}

@article{MTMT:34130083,
	title = {Oxidative-Stress-Related Alterations in Metabolic Panel, Red Blood Cell Indices, and Erythrocyte Morphology in a Type 1 Diabetic Rat Model},
	url = {https://m2.mtmt.hu/api/publication/34130083},
	author = {Szalai, Zita and Magyariné, Berkó Anikó and Bódi, Nikolett and Hermesz, Edit and Ferencz, Ágnes and Bagyánszki, Mária},
	doi = {10.3390/app13179920},
	journal-iso = {APPL SCI-BASEL},
	journal = {APPLIED SCIENCES-BASEL},
	volume = {13},
	unique-id = {34130083},
	abstract = {Diabetes mellitus is often associated with vascular complications in which hyperglycemia-induced oxidative stress may be the cause of the impaired vessels and circulating blood cells. The aim of this study was to follow the hyperglycemia-related metabolic and morphological changes in blood and urine samples of Wistar rats. Animals were divided into streptozotocin-induced diabetic (acute and chronic), insulin-treated diabetic, reversed diabetic, and control groups. In chronic diabetic rats, decreases in albumin, total protein, and antioxidant glutation concentration were measured, while glutamic-pyruvic transaminase, alkaline phosphatase, red blood cell (RBC) count, hematocrit, and hemoglobin levels were increased. Moreover, an increased level of the phenotypic variants was detected in the RBC population of the diabetic animals. In conclusion, we verified the sensitivity of RBCs to long-lasting hyperglycemia, and to insulin deficiency, which were both accompanied with an increased level of RBC-derived parameters and the presence of eccentrocytes, hemolyzed RBCs, and codocytes. Moreover, our results show that the response of the RBC glutation system to oxidative stress depends on the duration of hyperglycemia, and that the short-term activation of this defense system is exhausted in a long-lasting oxidative environment. Insulin therapy was effective in the case of most parameters, which clearly emphasizes the importance of maintaining blood glucose at physiological level.},
	year = {2023},
	eissn = {2076-3417},
	orcid-numbers = {Szalai, Zita/0000-0002-8722-0211; Magyariné, Berkó Anikó/0000-0002-1237-5745; Bódi, Nikolett/0000-0002-9774-1387; Hermesz, Edit/0000-0002-0543-6693; Ferencz, Ágnes/0000-0002-4149-4698; Bagyánszki, Mária/0000-0003-3533-9461}
}

@article{MTMT:33288108,
	title = {Molecular Background of Toxic-Substances-Induced Morphological Alterations in the Umbilical Cord Vessels and Fetal Red Blood Cells},
	url = {https://m2.mtmt.hu/api/publication/33288108},
	author = {Zahorán, Szabolcs and Márton, Ágnes and Dugmonits, Krisztina Nikoletta and Chakraborty, Payal and Khamit, Ali and Hegyi, Péter and Orvos, Hajnalka and Hermesz, Edit},
	doi = {10.3390/ijms232314673},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {33288108},
	issn = {1661-6596},
	abstract = {The relationship between smoking and human health has been investigated mostly in adults, despite the fact that the chemicals originating from sustained maternal smoking disrupt the carefully orchestrated regulatory cascades in the developing fetus. In this study, we followed molecular alterations in the umbilical cord (UC) vessels and fetal red blood cells (RBCs), which faithfully reflect the in vivo status of the fetus. We showed evidence for the decreased level of DNA-PKcs-positive nuclei in samples with smoking origin, which is associated with the impaired DNA repair system. Furthermore, we pointed out the altered ratio of MMP-9 metalloproteinase and its endogenous inhibitor TIMP-1, which might be a possible explanation for the morphological abnormalities in the UC vessels. The presented in vivo dataset emphasizes the higher vulnerability of the veins, as the primary target for the toxic materials unfiltered by the placenta. All these events become amplified by the functionally impaired fetal RBC population via a crosstalk mechanism between the vessel endothelium and the circulating RBCs. In our ex vivo approach, we looked for the molecular explanation of metal-exposure-induced alterations, where expressions of the selected genes were upregulated in the control group, while samples with smoking origin showed a lack of response, indicative of prior long-term in utero exposure.},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Zahorán, Szabolcs/0000-0002-6649-8249; Dugmonits, Krisztina Nikoletta/0000-0003-3482-7578; Khamit, Ali/0000-0002-5405-7702; Hegyi, Péter/0000-0003-0399-7259; Orvos, Hajnalka/0000-0001-9400-865X; Hermesz, Edit/0000-0002-0543-6693}
}

@article{MTMT:32024346,
	title = {Diabetes-related intestinal region-specific thickening of ganglionic basement membrane and regionally decreased matrix metalloproteinase 9 expression in myenteric ganglia},
	url = {https://m2.mtmt.hu/api/publication/32024346},
	author = {Bódi, Nikolett and Mezei, Diána and Chakraborty, Payal and Szalai, Zita and Barta, Bence Pál and Balázs, János and Rázga, Zsolt and Hermesz, Edit and Bagyánszki, Mária},
	doi = {10.4239/wjd.v12.i5.658},
	journal-iso = {WORLD J DIABETES},
	journal = {WORLD JOURNAL OF DIABETES},
	volume = {12},
	unique-id = {32024346},
	abstract = {BACKGROUND
		The importance of the neuronal microenvironment has been recently highlighted in gut region-specific diabetic enteric neuropathy. Regionally distinct thickening of endothelial basement membrane (BM) of intestinal capillaries supplying the myenteric ganglia coincide with neuronal damage in different intestinal segments. Accelerated synthesis of matrix molecules and reduced degradation of matrix components may also contribute to the imbalance of extracellular matrix dynamics resulting in BM thickening. Among the matrix degrading proteinases, matrix metalloproteinase 9 (MMP9) and its tissue inhibitor (TIMP1) are essential in regulating extracellular matrix remodelling.
		
		AIM
		To evaluate the intestinal segment-specific effects of diabetes and insulin replacement on ganglionic BM thickness, MMP9 and TIMP1 expression.
		
		METHODS
		Ten weeks after the onset of hyperglycaemia gut segments were taken from the duodenum and ileum of streptozotocin-induced diabetic, insulin-treated diabetic and sex- and age-matched control rats. The thickness of BM surrounding myenteric ganglia was measured by electron microscopic morphometry. Whole-mount preparations of myenteric plexus were prepared from the different gut regions for MMP9/TIMP1 double-labelling fluorescent immunohistochemistry. Post-embedding immunogold electron microscopy was applied on ultrathin sections to evaluate the MMP9 and TIMP1 expression in myenteric ganglia and their microenvironment from different gut segments and conditions. The MMP9 and TIMP1 messenger ribonucleic acid (mRNA) level was measured by quantitative polymerase chain reaction.
		
		RESULTS
		Ten weeks after the onset of hyperglycaemia, the ganglionic BM was significantly thickened in the diabetic ileum, while it remained intact in the duodenum. The immediate insulin treatment prevented the diabetes-related thickening of the BM surrounding the ileal myenteric ganglia. Quantification of particle density showed an increasing tendency for MMP9 and a decreasing tendency for TIMP1 from the proximal to the distal small intestine under control conditions. In the diabetic ileum, the number of MMP9-indicating gold particles decreased in myenteric ganglia, endothelial cells of capillaries and intestinal smooth muscle cells, however, it remained unchanged in all duodenal compartments. The MMP9/TIMP1 ratio was also decreased in ileal ganglia only. However, a marked segment-specific induction was revealed in MMP9 and TIMP1 at the mRNA levels.
		
		CONCLUSION
		These findings support that the regional decrease in MMP9 expression in myenteric ganglia and their microenvironment may contribute to extracellular matrix accumulation, resulting in a region-specific thickening of ganglionic BM.},
	year = {2021},
	eissn = {1948-9358},
	pages = {658-672},
	orcid-numbers = {Bódi, Nikolett/0000-0002-9774-1387; Szalai, Zita/0000-0002-8722-0211; Barta, Bence Pál/0000-0002-5309-8633; Balázs, János/0000-0003-1775-6915; Rázga, Zsolt/0000-0003-4717-8482; Hermesz, Edit/0000-0002-0543-6693; Bagyánszki, Mária/0000-0003-3533-9461}
}

@article{MTMT:32150374,
	title = {Fetal oxygen supply can be improved by an effective cross-talk between fetal erythrocytes and vascular endothelium},
	url = {https://m2.mtmt.hu/api/publication/32150374},
	author = {Chakraborty, Payal and Khamit, Ali and Hermesz, Edit},
	doi = {10.1016/j.bbadis.2021.166243},
	journal-iso = {BBA-MOL BASIS DIS},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE},
	volume = {1867},
	unique-id = {32150374},
	issn = {0925-4439},
	year = {2021},
	eissn = {1879-260X},
	orcid-numbers = {Hermesz, Edit/0000-0002-0543-6693}
}

@article{MTMT:31969947,
	title = {Sustained maternal smoking triggers endothelial-mediated oxidative stress in the umbilical cord vessels, resulting in vascular dysfunction},
	url = {https://m2.mtmt.hu/api/publication/31969947},
	author = {Zahorán, S. and Szántó, P.R. and Bódi, Nikolett and Bagyánszki, Mária and Maléth, József and Hegyi, Péter and Sári, T. and Hermesz, Edit},
	doi = {10.3390/antiox10040583},
	journal-iso = {ANTIOXIDANTS-BASEL},
	journal = {ANTIOXIDANTS},
	volume = {10},
	unique-id = {31969947},
	abstract = {Nitric oxide (NO) bioavailability is fundamental in the regulation of redox balance and functionality of the endothelium, especially in the case of the umbilical cord (UC), which has no innervation. The analysis of UC vessel-related complications could serve as a useful tool in the understanding of the pathophysiological mechanisms leading to neonatal cardiovascular disorders. Therefore, the aim of this study was to characterize the mechanisms that rule the severity of prenatal endothelial dysfunction, induced by the long-term effect of maternal smoking. Our analysis describes the initiation and the consequences of endothelial nitric oxide synthase (NOS3) deactivation, along with the up-regulation of possible compensatory pathways, using structural, molecular and biochemical approaches. This study was carried out on both the UC arteries and veins originated from neonates born to non-smoking and heavy-smoking mothers. The alterations stimulated by maternal smoking are vessel-specific and proportional to the level of exposure to harmful materials passed through the placenta. Typically, in the primarily exposed veins, an increased formation of reactive oxygen species and an up-regulation of the highly-efficient NOS2-NO producing pathway were detected. Despite all the extensive structural and functional damages, the ex vivo heat and cadmium ion-treated UC vein pieces still support the potential for stress response.},
	year = {2021},
	eissn = {2076-3921},
	orcid-numbers = {Bódi, Nikolett/0000-0002-9774-1387; Bagyánszki, Mária/0000-0003-3533-9461; Maléth, József/0000-0001-5768-3090; Hegyi, Péter/0000-0003-0399-7259; Hermesz, Edit/0000-0002-0543-6693}
}

@article{MTMT:31126626,
	title = {Sustained maternal smoking-associated changes in the physico-chemical properties of fetal RBC membranes might serve as early markers for vascular comorbidities},
	url = {https://m2.mtmt.hu/api/publication/31126626},
	author = {Balogh, Gábor and Chakraborty, Payal and Dugmonits, Krisztina Nikoletta and Péter, Mária and Végh, Attila Gergely and Vigh, László and Hermesz, Edit},
	doi = {10.1016/j.bbalip.2020.158615},
	journal-iso = {BBA-MOL CELL BIOL L},
	journal = {BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS},
	volume = {1865},
	unique-id = {31126626},
	issn = {1388-1981},
	year = {2020},
	eissn = {1879-2618},
	orcid-numbers = {Dugmonits, Krisztina Nikoletta/0000-0003-3482-7578; Végh, Attila Gergely/0000-0003-0524-0946; Hermesz, Edit/0000-0002-0543-6693}
}

@article{MTMT:31646685,
	title = {Mature Twin Neonates Exhibit Oxidative Stress via Nitric Oxide Synthase Dysfunctionality. A Prognostic Stress Marker in the Red Blood Cells and Umbilical Cord Vessels},
	url = {https://m2.mtmt.hu/api/publication/31646685},
	author = {Chakraborty, Payal and Dugmonits, Krisztina Nikoletta and Orvos, Hajnalka and Hermesz, Edit},
	doi = {10.3390/antiox9090845},
	journal-iso = {ANTIOXIDANTS-BASEL},
	journal = {ANTIOXIDANTS},
	volume = {9},
	unique-id = {31646685},
	year = {2020},
	eissn = {2076-3921},
	orcid-numbers = {Dugmonits, Krisztina Nikoletta/0000-0003-3482-7578; Orvos, Hajnalka/0000-0001-9400-865X; Hermesz, Edit/0000-0002-0543-6693}
}

@article{MTMT:31266365,
	title = {Response of Human Neutrophil Granulocytes to the Hyphae of the Emerging Fungal Pathogen Curvularia lunata},
	url = {https://m2.mtmt.hu/api/publication/31266365},
	author = {Tóth, Eszter Judit and Varga, Mónika and Takó, Miklós and Homa, Mónika and Jáger, Olivér and Hermesz, Edit and Orvos, Hajnalka and Nagy, Gábor and Vágvölgyi, Csaba and Papp, Tamás},
	doi = {10.3390/pathogens9030235},
	journal-iso = {PATHOGENS},
	journal = {PATHOGENS},
	volume = {9},
	unique-id = {31266365},
	year = {2020},
	eissn = {2076-0817},
	orcid-numbers = {Takó, Miklós/0000-0002-1219-1049; Homa, Mónika/0000-0002-2724-4713; Hermesz, Edit/0000-0002-0543-6693; Orvos, Hajnalka/0000-0001-9400-865X; Nagy, Gábor/0000-0002-7871-6098; Vágvölgyi, Csaba/0000-0003-0009-7773; Papp, Tamás/0000-0001-8211-5431}
}