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Article ; Online: Co-Expression and Functional Interactions of Death Receptor 3 and E-Selectin in Clear Cell Renal Cell Carcinoma.

Al-Lamki, Rafia S / Wang, Jun / Pober, Jordan S / Bradley, John R

2022 Volume 192, Issue 4, Page(s) 722–736

Abstract: Similar to the behavior of inflamed tubular epithelial cells, clear cell renal cell carcinoma (ccRCC) cells express death receptor 3 (DR3 or TNFSFR25) in situ, and expression increases with tumor grade. Surprisingly, E-selectin, which can be induced in ... ...

Abstract	Similar to the behavior of inflamed tubular epithelial cells, clear cell renal cell carcinoma (ccRCC) cells express death receptor 3 (DR3 or TNFSFR25) in situ, and expression increases with tumor grade. Surprisingly, E-selectin, which can be induced in endothelial cells by DR3 signaling, is also expressed by ccRCC cells and increases with tumor grade. In ccRCC organ cultures, addition of tumor necrosis factor-like 1A (TL1A or TNFSF15), the ligand for DR3, activates NF-κB and mitogen-activated protein kinases, induces both DR3 and E-selectin expression in an NF-κB-dependent manner, and promotes cell cycle entry. DR3 immunoprecipitated from ccRCC tissue contains sialyl Lewis X moieties (the ligand recognized by E-selectin), proximity ligation assays reveal DR3, and E-selectin interacts on ccRCC cells. Similar to that with the addition of TL1A, the addition of soluble E-selectin to ccRCC organ cultures activates NF-κB and mitogen-activated protein kinases in ccRCC cells and increases both DR3 and E-selectin expression and cell-cycle entry. In contrast, normal renal tubular epithelium, which poorly expresses DR3, is minimally responsive to either of these ligands. These data suggest a functional role for autocrine/paracrine DR3/E-selectin interactions in ccRCC and its progression, revealing a potential new target for therapeutic intervention.
MeSH term(s)	Antigens, CD ; Carcinoma, Renal Cell/metabolism ; E-Selectin/genetics ; E-Selectin/metabolism ; Endothelial Cells/metabolism ; Female ; Humans ; Kidney Neoplasms/metabolism ; Ligands ; Male ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/metabolism ; Receptors, Tumor Necrosis Factor, Member 25/genetics ; Receptors, Tumor Necrosis Factor, Member 25/metabolism ; Tumor Necrosis Factor Ligand Superfamily Member 15/metabolism
Chemical Substances	Antigens, CD ; E-Selectin ; Ligands ; NF-kappa B ; Receptors, Tumor Necrosis Factor, Member 25 ; SELE protein, human ; TNFRSF25 protein, human ; TNFSF15 protein, human ; Tumor Necrosis Factor Ligand Superfamily Member 15 ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2022-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2021.12.010
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Article ; Online: Williams syndrome.

Kozel, Beth A / Barak, Boaz / Kim, Chong Ae / Mervis, Carolyn B / Osborne, Lucy R / Porter, Melanie / Pober, Barbara R

Nature reviews. Disease primers

2021 Volume 7, Issue 1, Page(s) 42

Abstract: Williams syndrome (WS) is a relatively rare microdeletion disorder that occurs in as many as 1:7,500 individuals. WS arises due to the mispairing of low-copy DNA repetitive elements at meiosis. The deletion size is similar across most individuals with WS ...

Abstract	Williams syndrome (WS) is a relatively rare microdeletion disorder that occurs in as many as 1:7,500 individuals. WS arises due to the mispairing of low-copy DNA repetitive elements at meiosis. The deletion size is similar across most individuals with WS and leads to the loss of one copy of 25-27 genes on chromosome 7q11.23. The resulting unique disorder affects multiple systems, with cardinal features including but not limited to cardiovascular disease (characteristically stenosis of the great arteries and most notably supravalvar aortic stenosis), a distinctive craniofacial appearance, and a specific cognitive and behavioural profile that includes intellectual disability and hypersociability. Genotype-phenotype evidence is strongest for ELN, the gene encoding elastin, which is responsible for the vascular and connective tissue features of WS, and for the transcription factor genes GTF2I and GTF2IRD1, which are known to affect intellectual ability, social functioning and anxiety. Mounting evidence also ascribes phenotypic consequences to the deletion of BAZ1B, LIMK1, STX1A and MLXIPL, but more work is needed to understand the mechanism by which these deletions contribute to clinical outcomes. The age of diagnosis has fallen in regions of the world where technological advances, such as chromosomal microarray, enable clinicians to make the diagnosis of WS without formally suspecting it, allowing earlier intervention by medical and developmental specialists. Phenotypic variability is considerable for all cardinal features of WS but the specific sources of this variability remain unknown. Further investigation to identify the factors responsible for these differences may lead to mechanism-based rather than symptom-based therapies and should therefore be a high research priority.
MeSH term(s)	Cognition ; Elastin ; Humans ; Transcription Factors ; Williams Syndrome/diagnosis ; Williams Syndrome/genetics
Chemical Substances	BAZ1B protein, human ; Transcription Factors ; Elastin (9007-58-3)
Language	English
Publishing date	2021-06-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	2056-676X
ISSN (online)	2056-676X
DOI	10.1038/s41572-021-00276-z
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Article ; Online: Genetic aspects of human congenital diaphragmatic hernia.

Pober, B R

Clinical genetics

2008 Volume 74, Issue 1, Page(s) 1–15

Abstract: Congenital diaphragmatic hernia (CDH) is a common major malformation affecting 1/3000-1/4000 births, which continues to be associated with significant perinatal mortality. Much current research is focused on elucidating the genetics and pathophysiology ... ...

Abstract	Congenital diaphragmatic hernia (CDH) is a common major malformation affecting 1/3000-1/4000 births, which continues to be associated with significant perinatal mortality. Much current research is focused on elucidating the genetics and pathophysiology contributing to CDH to develop more effective therapies. The latest data suggest that many cases of CDH are genetically determined and also indicate that CDH is etiologically heterogeneous. The present review will provide a brief summary of diaphragm development and model organism work most relevant to human CDH and will primarily describe important human phenotypes associated with CDH and also provide recommendations for diagnostic evaluation of a fetus or infant with CDH.
MeSH term(s)	Animals ; Chromosome Aberrations ; Diaphragm/embryology ; Diaphragm/growth & development ; Disease Models, Animal ; Hernia, Diaphragmatic/genetics ; Hernias, Diaphragmatic, Congenital ; Humans ; Mice
Language	English
Publishing date	2008-05-28
Publishing country	Denmark
Document type	Journal Article ; Review
ZDB-ID	221209-2
ISSN	1399-0004 ; 0009-9163
ISSN (online)	1399-0004
ISSN	0009-9163
DOI	10.1111/j.1399-0004.2008.01031.x
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Article ; Online: Identification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis.

Moledina, Dennis G / Obeid, Wassim / Smith, Rex N / Rosales, Ivy / Sise, Meghan E / Moeckel, Gilbert / Kashgarian, Michael / Kuperman, Michael / Campbell, Kirk N / Lefferts, Sean / Meliambro, Kristin / Bitzer, Markus / Perazella, Mark A / Luciano, Randy L / Pober, Jordan S / Cantley, Lloyd G / Colvin, Robert B / Wilson, F Perry / Parikh, Chirag R

The Journal of clinical investigation

2024 Volume 134, Issue 6

MeSH term(s)	Humans ; Nephritis, Interstitial/diagnosis ; Biomarkers ; Acute Disease ; Chemokine CXCL9
Chemical Substances	Biomarkers ; CXCL9 protein, human ; Chemokine CXCL9
Language	English
Publishing date	2024-03-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI180583
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Article ; Online: Description of common musculoskeletal findings in Williams Syndrome and implications for therapies.

Copes, L E / Pober, B R / Terilli, C A

Clinical anatomy (New York, N.Y.)

2016 Volume 29, Issue 5, Page(s) 578–589

Abstract: Williams syndrome (WS), also referred to as Williams-Beuren syndrome (WBS), is a relatively rare genetic disorder affecting ∼1/10,000 persons. Since the disorder is caused by a micro-deletion of ∼1.5 Mb, it is not surprising that the manifestations of WS ...

Abstract	Williams syndrome (WS), also referred to as Williams-Beuren syndrome (WBS), is a relatively rare genetic disorder affecting ∼1/10,000 persons. Since the disorder is caused by a micro-deletion of ∼1.5 Mb, it is not surprising that the manifestations of WS are extremely broad, involving most body systems. In this paper, we primarily focus on the musculoskeletal aspects of WS as these findings have not been the subject of a comprehensive review. We review the MSK features commonly seen in individuals with WS, along with related sensory and neurological issues interacting with and compounding underlying MSK abnormalities. We end by providing perspective, particularly from the vantage point of a physical therapist, on therapeutic interventions to address the most common MSK and related features seen in WS. Clin. Anat. 29:578-589, 2016. © 2016 Wiley Periodicals, Inc.
MeSH term(s)	Humans ; Musculoskeletal Abnormalities/etiology ; Physical Therapy Modalities ; Williams Syndrome/complications ; Williams Syndrome/pathology ; Williams Syndrome/therapy
Language	English
Publishing date	2016-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1025505-9
ISSN	1098-2353 ; 0897-3806
ISSN (online)	1098-2353
ISSN	0897-3806
DOI	10.1002/ca.22685
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Article ; Online: Matrisome and Immune Pathways Contribute to Extreme Vascular Outcomes in Williams-Beuren Syndrome.

Liu, Delong / Billington, Charles J / Raja, Neelam / Wong, Zoe C / Levin, Mark D / Resch, Wulfgang / Alba, Camille / Hupalo, Daniel N / Biamino, Elisa / Bedeschi, Maria Francesca / Digilio, Maria Cristina / Squeo, Gabriella Maria / Villa, Roberta / Parrish, Pheobe C R / Knutsen, Russell H / Osgood, Sharon / Freeman, Joy A / Dalgard, Clifton L / Merla, Giuseppe /

Pober, Barbara R / Mervis, Carolyn B / Roberts, Amy E / Morris, Colleen A / Osborne, Lucy R / Kozel, Beth A

Journal of the American Heart Association

2024 Volume 13, Issue 3, Page(s) e031377

Abstract: Background: Supravalvar aortic stenosis (SVAS) is a characteristic feature of Williams-Beuren syndrome (WBS). Its severity varies: ~20% of people with Williams-Beuren syndrome have SVAS requiring surgical intervention, whereas ~35% have no appreciable ... ...

Abstract	Background: Supravalvar aortic stenosis (SVAS) is a characteristic feature of Williams-Beuren syndrome (WBS). Its severity varies: ~20% of people with Williams-Beuren syndrome have SVAS requiring surgical intervention, whereas ~35% have no appreciable SVAS. The remaining individuals have SVAS of intermediate severity. Little is known about genetic modifiers that contribute to this variability. Methods and results: We performed genome sequencing on 473 individuals with Williams-Beuren syndrome and developed strategies for modifier discovery in this rare disease population. Approaches include extreme phenotyping and nonsynonymous variant prioritization, followed by gene set enrichment and pathway-level association tests. We next used GTEx v8 and proteomic data sets to verify expression of candidate modifiers in relevant tissues. Finally, we evaluated overlap between the genes/pathways identified here and those ascertained through larger aortic disease/trait genome-wide association studies. We show that SVAS severity in Williams-Beuren syndrome is associated with increased frequency of common and rarer variants in matrisome and immune pathways. Two implicated matrisome genes ( Conclusions: Smaller sample sizes in rare disease studies necessitate new approaches to detect modifiers. Our strategies identified variation in matrisome and immune pathways that are associated with SVAS severity. These findings suggest that, like other aortopathies, SVAS may be influenced by the balance of synthesis and degradation of matrisome proteins. Leveraging multiomic data and results from larger aorta-focused genome-wide association studies may accelerate modifier discovery for rare aortopathies like SVAS.
MeSH term(s)	Humans ; Williams Syndrome/genetics ; Genome-Wide Association Study ; Proteomics ; Rare Diseases ; Aortic Stenosis, Supravalvular/genetics ; Aortic Stenosis, Supravalvular/metabolism ; Aortic Stenosis, Supravalvular/surgery
Language	English
Publishing date	2024-01-31
Publishing country	England
Document type	Journal Article
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.123.031377
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Article ; Online: Rheumatoid arthritis T cell and muscle oxidative metabolism associate with exercise-induced changes in cardiorespiratory fitness.

Andonian, Brian J / Koss, Alec / Koves, Timothy R / Hauser, Elizabeth R / Hubal, Monica J / Pober, David M / Lord, Janet M / MacIver, Nancie J / St Clair, E William / Muoio, Deborah M / Kraus, William E / Bartlett, David B / Huffman, Kim M

Scientific reports

2022 Volume 12, Issue 1, Page(s) 7450

Abstract: Rheumatoid arthritis (RA) T cells drive autoimmune features via metabolic reprogramming that reduces oxidative metabolism. Exercise training improves cardiorespiratory fitness (i.e., systemic oxidative metabolism) and thus may impact RA T cell oxidative ... ...

Abstract	Rheumatoid arthritis (RA) T cells drive autoimmune features via metabolic reprogramming that reduces oxidative metabolism. Exercise training improves cardiorespiratory fitness (i.e., systemic oxidative metabolism) and thus may impact RA T cell oxidative metabolic function. In this pilot study of RA participants, we took advantage of heterogeneous responses to a high-intensity interval training (HIIT) exercise program to identify relationships between improvements in cardiorespiratory fitness with changes in peripheral T cell and skeletal muscle oxidative metabolism. In 12 previously sedentary persons with seropositive RA, maximal cardiopulmonary exercise tests, fasting blood, and vastus lateralis biopsies were obtained before and after 10 weeks of HIIT. Following HIIT, improvements in RA cardiorespiratory fitness were associated with changes in RA CD4 + T cell basal and maximal respiration and skeletal muscle carnitine acetyltransferase (CrAT) enzyme activity. Further, changes in CD4 + T cell respiration were associated with changes in naïve CD4 + CCR7 + CD45RA + T cells, muscle CrAT, and muscle medium-chain acylcarnitines and fat oxidation gene expression profiles. In summary, modulation of cardiorespiratory fitness and molecular markers of skeletal muscle oxidative metabolism during exercise training paralleled changes in T cell metabolism. Exercise training that improves RA cardiorespiratory fitness may therefore be valuable in managing pathologically related immune and muscle dysfunction.Trial registration: ClinicalTrials.gov, NCT02528344. Registered on 19 August 2015.
MeSH term(s)	Arthritis, Rheumatoid/metabolism ; Cardiorespiratory Fitness ; Humans ; Muscle, Skeletal/metabolism ; Oxidative Stress ; Pilot Projects
Language	English
Publishing date	2022-05-06
Publishing country	England
Document type	Clinical Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-11458-4
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Article ; Online: Identification and validation of urinary CXCL9 as a biomarker for diagnosis of acute interstitial nephritis.

The Journal of clinical investigation

2023 Volume 133, Issue 13

Abstract: BackgroundAcute tubulointerstitial nephritis (AIN) is one of the few causes of acute kidney injury with diagnosis-specific treatment options. However, due to the need to obtain a kidney biopsy for histological confirmation, AIN diagnosis can be delayed, ... ...

Abstract	BackgroundAcute tubulointerstitial nephritis (AIN) is one of the few causes of acute kidney injury with diagnosis-specific treatment options. However, due to the need to obtain a kidney biopsy for histological confirmation, AIN diagnosis can be delayed, missed, or incorrectly assumed. Here, we identify and validate urinary CXCL9, an IFN-γ-induced chemokine involved in lymphocyte chemotaxis, as a diagnostic biomarker for AIN.MethodsIn a prospectively enrolled cohort with pathologist-adjudicated histological diagnoses, termed the discovery cohort, we tested the association of 180 immune proteins measured by an aptamer-based assay with AIN and validated the top protein, CXCL9, using sandwich immunoassay. We externally validated these findings in 2 cohorts with biopsy-confirmed diagnoses, termed the validation cohorts, and examined mRNA expression differences in kidney tissue from patients with AIN and individuals in the control group.ResultsIn aptamer-based assay, urinary CXCL9 was 7.6-fold higher in patients with AIN than in individuals in the control group (P = 1.23 × 10-5). Urinary CXCL9 measured by sandwich immunoassay was associated with AIN in the discovery cohort (n = 204; 15% AIN) independently of currently available clinical tests for AIN (adjusted odds ratio for highest versus lowest quartile: 6.0 [1.8-20]). Similar findings were noted in external validation cohorts, where CXCL9 had an AUC of 0.94 (0.86-1.00) for AIN diagnosis. CXCL9 mRNA expression was 3.9-fold higher in kidney tissue from patients with AIN (n = 19) compared with individuals in the control group (n = 52; P = 5.8 × 10-6).ConclusionWe identified CXCL9 as a diagnostic biomarker for AIN using aptamer-based urine proteomics, confirmed this association using sandwich immunoassays in discovery and external validation cohorts, and observed higher expression of this protein in kidney biopsies from patients with AIN.FundingThis study was supported by National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) awards K23DK117065 (DGM), K08DK113281 (KM), R01DK128087 (DGM), R01DK126815 (DGM and LGC), R01DK126477 (KNC), UH3DK114866 (CRP, DGM, and FPW), R01DK130839 (MES), and P30DK079310 (the Yale O'Brien Center). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
MeSH term(s)	Humans ; Nephritis, Interstitial/diagnosis ; Nephritis, Interstitial/chemically induced ; Nephritis, Interstitial/pathology ; Kidney/pathology ; Biomarkers ; RNA, Messenger ; Chemokine CXCL9/genetics ; Chemokine CXCL9/adverse effects
Chemical Substances	Biomarkers ; RNA, Messenger ; CXCL9 protein, human ; Chemokine CXCL9
Language	English
Publishing date	2023-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI168950
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Article ; Online: Mild macrocytosis in Williams-Beuren syndrome.

Yu, Eric / Feinn, Richard / Bona, Robert / Brink, Benjamin / Sindhar, Sampat / Kozel, Beth A / Pober, Barbara R

European journal of medical genetics

2019 Volume 63, Issue 3, Page(s) 103740

Abstract: Objective: To evaluate the occurrence and estimate the frequency of macrocytosis in Williams-Beuren syndrome (WBS).: Study design: Complete blood count (CBC) data from 179 subjects with WBS aged 1-69 were collected, with common parameters assessed ... ...

Abstract	Objective: To evaluate the occurrence and estimate the frequency of macrocytosis in Williams-Beuren syndrome (WBS). Study design: Complete blood count (CBC) data from 179 subjects with WBS aged 1-69 were collected, with common parameters assessed for trends. Z-transformed mean corpuscular volume (MCV) was compared with each laboratory's reference range as well as with control data from the National Health and Nutrition Examination Survey (NHANES) 2013-2014 data archives. Results: Just over a third (35%) subjects had at least one recorded incidence of macrocytosis. In comparisons of CBC parameters with an expected population mean, MCV and MCH were greater than, while Hct and RDW were lower than, expected values. The distribution of erythrocyte MCV is shifted to the right in WBS compared to controls, as was the mean value. Despite this, anemia was absent, except in a single medically complex WBS subject. Though there was a paucity of data available of variables that could potentially cause an elevated MCV, no obvious etiology could be elucidated. Conclusions: Mild macrocytosis without anemia affects a moderate subset of WBS patients, leading to a rightward shift in the MCV distribution curve. Providers encountering isolated mild macrocytosis in WBS can consider observation over further workup.
MeSH term(s)	Adolescent ; Adult ; Aged ; Anemia ; Blood Cell Count ; Child ; Child, Preschool ; Cohort Studies ; Erythrocyte Indices ; Erythrocytes/cytology ; Erythrocytes/metabolism ; Female ; Hematologic Diseases/blood ; Hematologic Diseases/metabolism ; Humans ; Infant ; Male ; Middle Aged ; Williams Syndrome/blood ; Williams Syndrome/etiology ; Williams Syndrome/genetics ; Williams Syndrome/metabolism
Language	English
Publishing date	2019-08-14
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2184135-4
ISSN	1878-0849 ; 1769-7212
ISSN (online)	1878-0849
ISSN	1769-7212
DOI	10.1016/j.ejmg.2019.103740
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Article ; Online: Rheumatoid arthritis T cell and muscle oxidative metabolism associate with exercise-induced changes in cardiorespiratory fitness

Brian J. Andonian / Alec Koss / Timothy R. Koves / Elizabeth R. Hauser / Monica J. Hubal / David M. Pober / Janet M. Lord / Nancie J. MacIver / E. William St Clair / Deborah M. Muoio / William E. Kraus / David B. Bartlett / Kim M. Huffman

Scientific Reports, Vol 12, Iss 1, Pp 1-

2022 Volume 13

Abstract: Abstract Rheumatoid arthritis (RA) T cells drive autoimmune features via metabolic reprogramming that reduces oxidative metabolism. Exercise training improves cardiorespiratory fitness (i.e., systemic oxidative metabolism) and thus may impact RA T cell ... ...

Abstract	Abstract Rheumatoid arthritis (RA) T cells drive autoimmune features via metabolic reprogramming that reduces oxidative metabolism. Exercise training improves cardiorespiratory fitness (i.e., systemic oxidative metabolism) and thus may impact RA T cell oxidative metabolic function. In this pilot study of RA participants, we took advantage of heterogeneous responses to a high-intensity interval training (HIIT) exercise program to identify relationships between improvements in cardiorespiratory fitness with changes in peripheral T cell and skeletal muscle oxidative metabolism. In 12 previously sedentary persons with seropositive RA, maximal cardiopulmonary exercise tests, fasting blood, and vastus lateralis biopsies were obtained before and after 10 weeks of HIIT. Following HIIT, improvements in RA cardiorespiratory fitness were associated with changes in RA CD4 + T cell basal and maximal respiration and skeletal muscle carnitine acetyltransferase (CrAT) enzyme activity. Further, changes in CD4 + T cell respiration were associated with changes in naïve CD4 + CCR7 + CD45RA + T cells, muscle CrAT, and muscle medium-chain acylcarnitines and fat oxidation gene expression profiles. In summary, modulation of cardiorespiratory fitness and molecular markers of skeletal muscle oxidative metabolism during exercise training paralleled changes in T cell metabolism. Exercise training that improves RA cardiorespiratory fitness may therefore be valuable in managing pathologically related immune and muscle dysfunction. Trial registration: ClinicalTrials.gov, NCT02528344. Registered on 19 August 2015.
Keywords	Medicine ; R ; Science ; Q
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
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