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Bibliografia publikacji pracowników
Państwowej Szkoły Wyższej w Białej Podlaskiej

Baza tworzona przez Bibliotekę Akademii Bialskiej im. Jana Pawła II.


Zapytanie: ŁAWIŃSKI MICHAŁ
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Nr opisu: ga Piotr^bPiotr^c^d^e^f^g^h^i ^m_^n_^oReliga Piotr^pReliga Piotr^rReliga^sPiotr^u^t^qReliga P^w^x0000026524^zReliga Piotr^aThornetr^rReliga^sPiotr^u^t^qReliga P^w^x0000026524^zReliga Piotr^aThorne
Autorzy: , , .
Tytuł czasopisma:
Charakterystyka merytoryczna:
Język publikacji:
Wskaźnik Impact Factor ISI: artykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://link.springer.com/article/10.1007/s12026-024-09514-4100^a0257-277X^bQ^e1559-0755^iX^jXY^kQ008122^a003^b003^c2024-08-08, 14:37^d2025-01-09, 14:44^e3022968802^f2929958795^aThe impact of BDNF and CD4 + T cell crosstalk on depression^aImmunologic Research^a2024^bVol. 72^cissue 5^dp.883--894^a0257-277X^b1559-0755^a2024/2025^a10.1007/s12026-024-09514-4^aPaszkiewicz, Justyna^cy^abrain-derived neurotrophic factor's (BDNF)^aKopia dostępna w Sekcji Bibliometrii.^aDepression represents a prevalent health concern since it affects approximately 350 million people of all ages worldwide [1, 2]. Both genders suffer from depression, albeit women are disproportionally affected by it more than men [3]. Notably, depression has the potential to impact individuals across various phases of their lifespan. Around 15% of adolescents aged 14 to 18 will encounter at least a single significant depressive episode [4]. Depression continues to be a concern within the elderly community. Namely, approximately 7% of individuals aged 60 and above experience symptoms of depression [5, 6]. These observations highlight that depression is pervasive in our society. Brain-derived neurotrophic factor's (BDNF) role in depression is highly affected by various factors [7,8,9]. BDNF is a neurotrophin known for its roles in synaptic plasticity, dendritic spine morphology, cognitive function, and mood regulation [10,11,12,13,14]. BDNF polymorphisms, such as Val66met, can significantly influence an individual's predisposition to depression [15,16,17,18,19,20]. Epigenetic alterations of BDNF, such as increase/decrease in DNA methylation at specific CpG sites, have recently emerged as relevant mechanisms promoting susceptibility to the development of depressive-like symptoms [21, 22]. These genetic and epigenetic factors are deeply intertwined with environmental influences, such as early-life experiences, social support, and exposure to stressors. Together, they contribute to the role of BDNF in the onset and progression of depression [23,24,25]. Recently, CD4 + T cells, a fundamental constituent of the adaptive immune system, have come under the attention of various research groups for their potential involvement in mediating neuroinflammatory processes that influence mood and cognition [26,27,28]. CD4 + T cells are a heterogeneous group of cells that include both pro- (e.g., Th1 and Th17) and anti-inflammatory cell types (e.g., Treg). CD4 + T cells can influence depression onset and development in various ways, including direct effects on neurons, astrocytes, and microglia through the production of cytokines and expressing receptors for molecules produced by brain cells [29,30,31,32,33]. BDNF seems to have a positive effect on CD4 + T cell proliferation and differentiation. However, our understanding of BDNF's effects on each cell type remains limited. Surprisingly, IL-17, which is produced by pro-inflammatory Th17 cells, and IL-4, which is produced by anti-inflammatory Tregs, both seem to increase BDNF production by astrocytes. The reason behind this counterintuitive phenomenon remains unknown. This review aims to investigate the mechanisms of interaction between CD4 + T cells and BDNF in the context of depression to acquire a deeper understanding of depression and the development of more effective therapies. Therefore, we first cover the role of BDNF in depression, followed by discussing what is currently known about the role of C^aCD4 + T cells^adepression
Punktacja ministerstwa:
Praca recenzowana
Słowa kluczowe ang.: ;
kuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://link.springer.com/article/10.1007/s12026-024-09514-4100^a0257-277X^bQ^e1559-0755^iX^jXY^kQ008122^a003^b003^c2024-08-08, 14:37^d2025-01-09, 14:44^e3022968802^f2929958795^aThe impact of BDNF and CD4 + T cell crosstalk on depression^aImmunologic Research^a2024^bVol. 72^cissue 5^dp.883--894^a0257-277X^b1559-0755^a2024/2025^a10.1007/s12026-024-09514-4^aPaszkiewicz, Justyna^cy^abrain-derived neurotrophic factor's (BDNF)^aKopia dostępna w Sekcji Bibliometrii.^aDepression represents a prevalent health concern since it affects approximately 350 million people of all ages worldwide [1, 2]. Both genders suffer from depression, albeit women are disproportionally affected by it more than men [3]. Notably, depression has the potential to impact individuals across various phases of their lifespan. Around 15% of adolescents aged 14 to 18 will encounter at least a single significant depressive episode [4]. Depression continues to be a concern within the elderly community. Namely, approximately 7% of individuals aged 60 and above experience symptoms of depression [5, 6]. These observations highlight that depression is pervasive in our society. Brain-derived neurotrophic factor's (BDNF) role in depression is highly affected by various factors [7,8,9]. BDNF is a neurotrophin known for its roles in synaptic plasticity, dendritic spine morphology, cognitive function, and mood regulation [10,11,12,13,14]. BDNF polymorphisms, such as Val66met, can significantly influence an individual's predisposition to depression [15,16,17,18,19,20]. Epigenetic alterations of BDNF, such as increase/decrease in DNA methylation at specific CpG sites, have recently emerged as relevant mechanisms promoting susceptibility to the development of depressive-like symptoms [21, 22]. These genetic and epigenetic factors are deeply intertwined with environmental influences, such as early-life experiences, social support, and exposure to stressors. Together, they contribute to the role of BDNF in the onset and progression of depression [23,24,25]. Recently, CD4 + T cells, a fundamental constituent of the adaptive immune system, have come under the attention of various research groups for their potential involvement in mediating neuroinflammatory processes that influence mood and cognition [26,27,28]. CD4 + T cells are a heterogeneous group of cells that include both pro- (e.g., Th1 and Th17) and anti-inflammatory cell types (e.g., Treg). CD4 + T cells can influence depression onset and development in various ways, including direct effects on neurons, astrocytes, and microglia through the production of cytokines and expressing receptors for molecules produced by brain cells [29,30,31,32,33]. BDNF seems to have a positive effect on CD4 + T cell proliferation and differentiation. However, our understanding of BDNF's effects on each cell type remains limited. Surprisingly, IL-17, which is produced by pro-inflammatory Th17 cells, and IL-4, which is produced by anti-inflammatory Tregs, both seem to increase BDNF production by astrocytes. The reason behind this counterintuitive phenomenon remains unknown. This review aims to investigate the mechanisms of interaction between CD4 + T cells and BDNF in the context of depression to acquire a deeper understanding of depression and the development of more effective therapies. Therefore, we first cover the role of BDNF in depression, followed by discussing what is currently known about the role of C^aCD4 + T cells^adepression

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Autorzy: , , .
Tytuł pracy:
Tytuł pracy w innym języku: F018328.00993999009994.1001422-0067003Investigation of Mutated in Colorectal Cancer (MCC) Gene Family Evolution History Indicates a Putative Role in Th17/Treg DifferentiationInternational Journal of Molecular Sciences20231422-00672022/202310.3390/ijms241511940Paszkiewicz, Justynacolorectal cancerWpływ endogennego rozszczelnienia bariery krew-mózg w patogenezie zróżnicowanej podatności na inokulowanego czerniaka u linii myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowejFINAL_PUBLISHEDThe MCC family of genes plays a role in colorectal cancer development through various immunological pathways, including the Th17/Treg axis. We have previously shown that MCC1 but not MCC2 plays a role in Treg differentiation. Our understanding of the genetic divergence patterns and evolutionary history of the MCC family in relation to its function, in general, and the Th17/Treg axis, in particular, remains incomplete. In this investigation, we explored 12 species' genomes to study the phylogenetic origin, structure, and functional specificity of this family. In vertebrates, both MCC1 and MCC2 homologs have been discovered, while invertebrates have a single MCC homolog. We found MCC homologs as early as Cnidarians and Trichoplax, suggesting that the MCC family first appeared 741 million years ago (Ma), whereas MCC divergence into the MCC1 and MCC2 families occurred at 540 Ma. In general, we did not detect significant positive selection regulating MCC evolution. Our investigation, based on MCC1 structural similarity, suggests that they may play a role in the evolutionary changes in Tregs' emergence towards complexity, including the ability to utilize calcium for differentiation through the use of the EFH calcium-binding domain. We also found that the motif NPSTGE was highly conserved in MCC1, but not in MCC2. The NPSTGE motif binds KEAP1 with high affinity, suggesting an Nrf2-mediated function for MCC1. In the case of MCC2, we found that the "modifier of rudimentary" motif is highly conserved. This motif contributes to the regulation of alternative splicing. Overall, our study sheds light on how the evolution of the MCC family is connected to its function in regulating the Th17/Treg axis.differentiationevolutionTh17Treg : Oryginalny artykuł naukowy : utrzymanie i rozwój potencjału badawczego - art. 365 pkt 2 ustawy : 998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM : 009859.000 : Q : 003 : Vol. 24 : Akademia Bialska im. Jana Pawła II w ramach Regulaminu wsparcia rozwoju zawodowego pracowników uczelni : CC-BY
Strony: F018328.00993999009994.1001422-0067003Investigation of Mutated in Colorectal Cancer (MCC) Gene Family Evolution History Indicates a Putative Role in Th17/Treg DifferentiationInternational Journal of Molecular Sciences20231422-00672022/202310.3390/ijms241511940Paszkiewicz, Justynacolorectal cancerWpływ endogennego rozszczelnienia bariery krew-mózg w patogenezie zróżnicowanej podatności na inokulowanego czerniaka u linii myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowejFINAL_PUBLISHEDThe MCC family of genes plays a role in colorectal cancer development through various immunological pathways, including the Th17/Treg axis. We have previously shown that MCC1 but not MCC2 plays a role in Treg differentiation. Our understanding of the genetic divergence patterns and evolutionary history of the MCC family in relation to its function, in general, and the Th17/Treg axis, in particular, remains incomplete. In this investigation, we explored 12 species' genomes to study the phylogenetic origin, structure, and functional specificity of this family. In vertebrates, both MCC1 and MCC2 homologs have bee, Oryginalny artykuł naukowy, utrzymanie i rozwój potencjału badawczego - art. 365 pkt 2 ustawy, 998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM, 009859.000, Q, 003, Vol. 24, Akademia Bialska im. Jana Pawła II w ramach Regulaminu wsparcia rozwoju zawodowego pracowników uczelni, CC-BY, 009999.000, 2023-09-29, 13:32, issue 15, y, PB/5/2022, AT_PUBLICATION, 009859.000202320232023Investigation of Mutated in Colorectal Cancer (MCC) Gene Family Evolution History Indicates a Put00000464160000000342AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1422-0067/24/15/11940100, 2024-06-25, 14:13, article number 11940
Seria: 8328.00993999009994.1001422-0067003, 998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM, 009859.000, Q, 003, 009999.000, 2023-09-29, 13: ; 009859.000202320232023Investigation of Mutated in Colorectal Cancer (MCC) Gene Family Evolution History Indicates a Put00000464160000000342AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1422-0067/24/15/11940100
Charakterystyka formalna: 22-0067^a2022/2023^a10.3390/ijms241511940^aPaszkiewicz, Justyna^cy^acolorectal cancer^aWpływ endogennego rozszczelnienia bariery krew-mózg w patogenezie zróżnicowanej podatności na inokulowanego czerniaka u linii myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowej^bAkademia Bialska im. Jana Pawła II w ramach Regulaminu wsparcia rozwoju zawodowego pracowników uczelni^cPB/5/2022^aFINAL_PUBLISHED^bCC-BY^cAT_PUBLICATION^eOPEN_JOURNAL^aThe MCC family of genes plays a role in colorectal cancer development through various immunological pathways, including the Th17/Treg axis. We have previously shown that MCC1 but not MCC2 plays a role in Treg differentiation. Our understanding of the genetic divergence patterns and evolutionary history of the MCC family in relation to its function, in general, and the Th17/Treg axis, in particular, remains incomplete. In this investigation, we explored 12 species' genomes to study the phylogenetic origin, structure, and functional specificity of this family. In vertebrates, both MCC1 and MCC2 homologs have been discovered, while invertebrates have a single MCC homolog. We found MCC homologs as early as Cnidarians and Trichoplax, suggesting that the MCC family first appeared 741 million years ago (Ma), whereas MCC divergence into the MCC1 and MCC2 families occurred at 540 Ma. In general, we did not detect significant positive selection regulating MCC evolution. Our investigation, based on MCC1 structural similarity, suggests that they may play a role in the evolutionary changes in Tregs' emergence towards complexity, including the ability to utilize calcium for differentiation through the use of the EFH calcium-binding domain. We also found that the motif NPSTGE was highly conserved in MCC1, but not in MCC2. The NPSTGE motif binds KEAP1 with high affinity, suggesting an Nrf2-mediated function for MCC1. In the case of MCC2, we found that the "modifier of rudimentary" motif is highly conserved. This motif contributes to the regulation of alternative splicing. Overall, our study sheds light on how the evolution of the MCC family is connected to its function in regulating the Th17/Treg axis.^adifferentiation^aevolution^aTh17^aTreg
Język publikacji: a2022/2023^a10.3390/ijms241511940^aPaszkiewicz, Justyna^cy^acolorectal cancer^aWpływ endogennego rozszczelnienia bariery krew-mózg w patogenezie zróżnicowanej podatności na inokulowanego czerniaka u linii myszy selekcjonowanych w kierunku wysokiej i niskiej analgezji postresowej^bAkademia Bialska im. Jana Pawła II w ramach Regulaminu wsparcia rozwoju zawodowego pracowników uczelni^cPB/5/2022^aFINAL_PUBLISHED^bCC-BY^cAT_PUBLICATION^eOPEN_JOURNAL^aThe MCC family of genes plays a role in colorectal cancer development through various immunological pathways, including the Th17/Treg axis. We have previously shown that MCC1 but not MCC2 plays a role in Treg differentiation. Our understanding of the genetic divergence patterns and evolutionary history of the MCC family in relation to its function, in general, and the Th17/Treg axis, in particular, remains incomplete. In this investigation, we explored 12 species' genomes to study the phylogenetic origin, structure, and functional specificity of this family. In vertebrates, both MCC1 and MCC2 homologs have been discovered, while invertebrates have a single MCC homolog. We found MCC homologs as early as Cnidarians and Trichoplax, suggesting that the MCC family first appeared 741 million years ago (Ma), whereas MCC divergence into the MCC1 and MCC2 families occurred at 540 Ma. In general, we did not detect significant positive selection regulating MCC evolution. Our investigation, based on MCC1 structural similarity, suggests that they may play a role in the evolutionary changes in Tregs' emergence towards complexity, including the ability to utilize calcium for differentiation through the use of the EFH calcium-binding domain. We also found that the motif NPSTGE was highly conserved in MCC1, but not in MCC2. The NPSTGE motif binds KEAP1 with high affinity, suggesting an Nrf2-mediated function for MCC1. In the case of MCC2, we found that the "modifier of rudimentary" motif is highly conserved. This motif contributes to the regulation of alternative splicing. Overall, our study sheds light on how the evolution of the MCC family is connected to its function in regulating the Th17/Treg axis.^adifferentiation^aevolution^aTh17^aTreg
Słowa kluczowe ang.:

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Autorzy: , , , .
Tytuł pracy:
Strony: RadziszewskiFraczekWolińskaPaszkiewiczReligaSacharczukF014101.00993999009994.1001422-0067003The Journey of Cancer Cells to the BrainInternational Journal of Molecular Sciences20231422-00672022/202310.3390/ijms24043854Paszkiewicz, JustynabraineFINAL_PUBLISHEDCancer metastases into the brain constitute one of the most severe, but not uncommon, manifestations of cancer progression. Several factors control how cancer cells interact with the brain to establish metastasis. These factors include mediators of signaling pathways participating in migration, infiltration of the blood-brain barrier, interaction with host cells (e.g., neurons, astrocytes), and the immune system. Development of novel therapies offers a glimpse of hope for increasing the diminutive life expectancy currently forecasted for patients suffering from brain metastasis. However, applying these treatment strategies has not been sufficiently effective. Therefore, there is a need for a better , Jakub, Karolina, Renata, Justyna, Piotr, Mariusz, utrzymanie i rozwój potencjału badawczego - art. 365 pkt 2 ustawy, 998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM, 009859.000, Q, 003, Challenges and Opportunities, Vol. 24, CC-BY, , , , 017, , , 009999.000, 2023-03-15, 10:29, issue 4, y, AT_PUBLICATION, , , , WNZS0101, , , 009859.000202320232023Journey of Cancer Cells to the Brain Challenges and Opportunities00000450840000000466AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1422-0067/24/4/3854100, 2024-06-25, 14:23, article number 3854
ISBN: Radziszewski
Charakterystyka formalna:
Język publikacji: arczuk Mariusz^bMariusz^c^d^e^f^g^h^i ^m_^n_^oSacharczuk Mariusz^pSacharczuk Mariusz^rSacharczuk^sMariusz^u^t^qSacharczuk M^w^x0000026532^zSacharczuk MariuszŁazarczyk Marzena Mickael Michel Edward Skiba Dominik Kurzejamska Ewa Ławiński Michał Horbańczuk Jarosław Olav^aF01^butrzymanie i rozwój potencjału badawczego - art. 365 pkt 2 ustawy^a4101.00^11ACZartykuł w czasopiśmie zagranicznym4.900IF^a993999^b998599140.0000140.000PUNKTACJA KBNPUNKTACJA MINISTERSTWALISTA FILADELFIJSKAIMPACT FACTOR140.000PUNKTACJA UWM^a009994.100^b009859.000^c009999.000^d009859.000202320232023Journey of Cancer Cells to the Brain Challenges and Opportunities00000450840000000466AOartykuł oryginalny naukowyPUBLIKACJAPEŁNA PUBLIKACJAAAartykuł w czasopiśmie z IF (wykaz MNiSW)AFILIACJA PODANAENGhttps://www.mdpi.com/1422-0067/24/4/3854100^a1422-0067^bQ^iX^jXY^kQ009159^a003^b003^c2023-03-15, 10:29^d2024-06-25, 14:23^e3127899210^f3024798816^aThe Journey of Cancer Cells to the Brain^bChallenges and Opportunities^aInternational Journal of Molecular Sciences^a2023^bVol. 24^cissue 4^darticle number 3854^a1422-0067^a2022/2023^a10.3390/ijms24043854^aPaszkiewicz, Justyna^cy^abraine^aFINAL_PUBLISHED^bCC-BY^cAT_PUBLICATION^eOPEN_JOURNAL^aCancer metastases into the brain constitute one of the most severe, but not uncommon, manifestations of cancer progression. Several factors control how cancer cells interact with the brain to establish metastasis. These factors include mediators of signaling pathways participating in migration, infiltration of the blood-brain barrier, interaction with host cells (e.g., neurons, astrocytes), and the immune system. Development of novel therapies offers a glimpse of hope for increasing the diminutive life expectancy currently forecasted for patients suffering from brain metastasis. However, applying these treatment strategies has not been sufficiently effective. Therefore, there is a need for a better understanding of the metastasis process to uncover novel therapeutic targets. In this review, we follow the journey of various cancer cells from their primary location through the diverse processes that they undergo to colonize the brain. These processes include EMT, intravasation, extravasation, and infiltration of the blood-brain barrier, ending up with colonization and angiogenesis. In each phase, we focus on the pathways engaging molecules that potentially could be drug target candidates.^acancer^aimmune cells^ametastasis
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