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Article ; Online: PEDF Deletion Induces Senescence and Defects in Phagocytosis in the RPE.

Rebustini, Ivan T / Crawford, Susan E / Becerra, S Patricia

International journal of molecular sciences

2022 Volume 23, Issue 14

Abstract: The retinal pigment epithelium (RPE) expresses ... ...

Abstract	The retinal pigment epithelium (RPE) expresses the
MeSH term(s)	Animals ; Cells, Cultured ; Eye Proteins/genetics ; Eye Proteins/metabolism ; Lipids ; Mice ; Mice, Knockout ; Nerve Growth Factors ; Phagocytosis/genetics ; Retinal Pigment Epithelium/metabolism ; Rhodopsin/metabolism ; Serpins/metabolism ; beta-Galactosidase/metabolism
Chemical Substances	Eye Proteins ; Lipids ; Nerve Growth Factors ; Serpins ; pigment epithelium-derived factor ; Rhodopsin (9009-81-8) ; beta-Galactosidase (EC 3.2.1.23)
Language	English
Publishing date	2022-07-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23147745
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Article ; Online: Antagonism Between PEDF and TGF-β Contributes to Type VI Osteogenesis Imperfecta Bone and Vascular Pathogenesis.

Kang, Heeseog / Aryal Ac, Smriti / Barnes, Aileen M / Martin, Aline / David, Valentin / Crawford, Susan E / Marini, Joan C

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

2022 Volume 37, Issue 5, Page(s) 925–937

Abstract: Osteogenesis imperfecta (OI) is a heterogeneous genetic disorder of bone and connective tissue, also known as brittle bone disease. Null mutations in SERPINF1, which encodes pigment epithelium-derived factor (PEDF), cause severe type VI OI, characterized ...

Abstract	Osteogenesis imperfecta (OI) is a heterogeneous genetic disorder of bone and connective tissue, also known as brittle bone disease. Null mutations in SERPINF1, which encodes pigment epithelium-derived factor (PEDF), cause severe type VI OI, characterized by accumulation of unmineralized osteoid and a fish-scale pattern of bone lamellae. Although the potent anti-angiogenic activity of PEDF has been extensively studied, the disease mechanism of type VI OI is not well understood. Using Serpinf1
MeSH term(s)	Animals ; Endothelial Cells ; Eye Proteins/genetics ; Eye Proteins/metabolism ; Mice ; Nerve Growth Factors/genetics ; Nerve Growth Factors/metabolism ; Osteogenesis Imperfecta/genetics ; Osteogenesis Imperfecta/metabolism ; Serpins/genetics ; Serpins/metabolism ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism
Chemical Substances	Eye Proteins ; Nerve Growth Factors ; Serpins ; Transforming Growth Factor beta ; pigment epithelium-derived factor
Language	English
Publishing date	2022-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	632783-7
ISSN	1523-4681 ; 0884-0431
ISSN (online)	1523-4681
ISSN	0884-0431
DOI	10.1002/jbmr.4540
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Zs.A 2142: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Gut-liver axis calibrates intestinal stem cell fitness.

Kim, Girak / Chen, Zuojia / Li, Jian / Luo, Jialie / Castro-Martinez, Felipe / Wisniewski, Jan / Cui, Kairong / Wang, Yan / Sun, Jialei / Ren, Xiaobai / Crawford, Susan E / Becerra, S Patricia / Zhu, Jimin / Liu, Taotao / Wang, Sui / Zhao, Keji / Wu, Chuan

Cell

2024 Volume 187, Issue 4, Page(s) 914–930.e20

Abstract: The gut and liver are recognized to mutually communicate through the biliary tract, portal vein, and systemic circulation. However, it remains unclear how this gut-liver axis regulates intestinal physiology. Through hepatectomy and transcriptomic and ... ...

Abstract	The gut and liver are recognized to mutually communicate through the biliary tract, portal vein, and systemic circulation. However, it remains unclear how this gut-liver axis regulates intestinal physiology. Through hepatectomy and transcriptomic and proteomic profiling, we identified pigment epithelium-derived factor (PEDF), a liver-derived soluble Wnt inhibitor, which restrains intestinal stem cell (ISC) hyperproliferation to maintain gut homeostasis by suppressing the Wnt/β-catenin signaling pathway. Furthermore, we found that microbial danger signals resulting from intestinal inflammation can be sensed by the liver, leading to the repression of PEDF production through peroxisome proliferator-activated receptor-α (PPARα). This repression liberates ISC proliferation to accelerate tissue repair in the gut. Additionally, treating mice with fenofibrate, a clinical PPARα agonist used for hypolipidemia, enhances colitis susceptibility due to PEDF activity. Therefore, we have identified a distinct role for PEDF in calibrating ISC expansion for intestinal homeostasis through reciprocal interactions between the gut and liver.
MeSH term(s)	Animals ; Mice ; Cell Proliferation ; Liver/metabolism ; PPAR alpha/metabolism ; Proteomics ; Stem Cells/metabolism ; Wnt Signaling Pathway ; Intestines/cytology ; Intestines/metabolism
Chemical Substances	PPAR alpha
Language	English
Publishing date	2024-01-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2024.01.001
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 58: Show issues

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Article ; Online: Loss of ephrin B2 receptor (EPHB2) sets lipid rheostat by regulating proteins DGAT1 and ATGL inducing lipid droplet storage in prostate cancer cells.

Morales, Alejandro / Greenberg, Max / Nardi, Francesca / Gil, Victoria / Hayward, Simon W / Crawford, Susan E / Franco, Omar E

Laboratory investigation; a journal of technical methods and pathology

2021 Volume 101, Issue 7, Page(s) 921–934

Abstract: Lipid droplet (LD) accumulation in cancer results from aberrant metabolic reprograming due to increased lipid uptake, diminished lipolysis and/or de novo lipid synthesis. Initially implicated in storage and lipid trafficking in adipocytes, LDs are more ... ...

Abstract	Lipid droplet (LD) accumulation in cancer results from aberrant metabolic reprograming due to increased lipid uptake, diminished lipolysis and/or de novo lipid synthesis. Initially implicated in storage and lipid trafficking in adipocytes, LDs are more recently recognized to fuel key functions associated with carcinogenesis and progression of several cancers, including prostate cancer (PCa). However, the mechanisms controlling LD accumulation in cancer are largely unknown. EPHB2, a tyrosine kinase (TKR) ephrin receptor has been proposed to have tumor suppressor functions in PCa, although the mechanisms responsible for these effects are unclear. Given that dysregulation in TRK signaling can result in glutaminolysis we postulated that EPHB2 might have potential effects on lipid metabolism. Knockdown strategies for EPHB2 were performed in prostate cancer cells to analyze the impact on the net lipid balance, proliferation, triacylglycerol-regulating proteins, effect on LD biogenesis, and intracellular localization of LDs. We found that EPHB2 protein expression in a panel of human-derived prostate cancer cell lines was inversely associated with in vivo cell aggressiveness. EPHB2 silencing increased the proliferation of prostate cancer cells and concurrently induced de novo LD accumulation in both cytoplasmic and nuclear compartments as well as a "shift" on LD size distribution in newly formed lipid-rich organelles. Lipid challenge using oleic acid exacerbated the effects on the LD phenotype. Loss of EPHB2 directly regulated key proteins involved in maintaining lipid homeostasis including, increasing lipogenic DGAT1, DGAT2 and PLIN2 and decreasing lipolytic ATGL and PEDF. A DGAT1-specific inhibitor abrogated LD accumulation and proliferative effects induced by EPHB2 loss. In conclusion, we highlight a new anti-tumor function of EPHB2 in lipid metabolism through regulation of DGAT1 and ATGL in prostate cancer. Blockade of DGAT1 in EPHB2-deficient tumors appears to be effective in restoring the lipid balance and reducing tumor growth.
MeSH term(s)	Cell Line, Tumor ; Diacylglycerol O-Acyltransferase/metabolism ; Humans ; Lipase/metabolism ; Lipid Droplets/metabolism ; Lipid Metabolism/physiology ; Male ; Prostatic Neoplasms/metabolism ; Receptor, EphB2/genetics ; Receptor, EphB2/metabolism
Chemical Substances	DGAT1 protein, human (EC 2.3.1.20) ; Diacylglycerol O-Acyltransferase (EC 2.3.1.20) ; EPHB2 protein, human (EC 2.7.10.1) ; Receptor, EphB2 (EC 2.7.10.1) ; Lipase (EC 3.1.1.3) ; PNPLA2 protein, human (EC 3.1.1.3)
Language	English
Publishing date	2021-04-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80178-1
ISSN	1530-0307 ; 0023-6837
ISSN (online)	1530-0307
ISSN	0023-6837
DOI	10.1038/s41374-021-00583-9
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Ud II Zs.164: Show issues

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Article: Correction: Elevated ATGL in colon cancer cells and cancer stem cells promotes metabolic and tumorigenic reprogramming reinforced by obesity.

Iftikhar, Rida / Penrose, Harrison M / King, Angelle N / Samudre, Joshua S / Collins, Morgan E / Hartono, Alifiani B / Lee, Sean B / Lau, Frank / Baddoo, Melody / Flemington, Erik F / Crawford, Susan E / Savkovic, Suzana D

Oncogenesis

2022 Volume 11, Issue 1, Page(s) 14

Language	English
Publishing date	2022-03-15
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2674437-5
ISSN	2157-9024
ISSN	2157-9024
DOI	10.1038/s41389-022-00388-5
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Article ; Online: Shared Inherited Genetics of Benign Prostatic Hyperplasia and Prostate Cancer.

Glaser, Alexander / Shi, Zhuqing / Wei, Jun / Lanman, Nadia A / Ladson-Gary, Skylar / Vickman, Renee E / Franco, Omar E / Crawford, Susan E / Lilly Zheng, S / Hayward, Simon W / Isaacs, William B / Helfand, Brian T / Xu, Jianfeng

European urology open science

2022 Volume 43, Page(s) 54–61

Abstract: Background: The association between benign prostatic hyperplasia (BPH) and prostate cancer (PCa) remains controversial, largely due to a detection bias in traditional observational studies.: Objective: To assess the association between BPH and PCa ... ...

Abstract	Background: The association between benign prostatic hyperplasia (BPH) and prostate cancer (PCa) remains controversial, largely due to a detection bias in traditional observational studies. Objective: To assess the association between BPH and PCa using inherited single nucleotide polymorphisms (SNPs). Design setting and participants: The participants were White men from the population-based UK Biobank (UKB). Outcome measurements and statistical analysis: The association between BPH and PCa was tested for (1) phenotypic correlation using chi-square, (2) genetic correlation ( Results and limitations: Among 214 717 White men in the UKB, 24 623 (11%) and 14 311 (6.7%) had a diagnosis of BPH and PCa, respectively. Diagnoses of these two diseases were significantly correlated (χ Conclusions: BPH and PCa share common inherited genetics, which suggests that the phenotypic association of these two diseases in observational studies is not entirely caused by the detection bias. Patient summary: For the first time, we found that benign prostatic hyperplasia and prostate cancer are genetically related. This finding may have implications in disease etiology and risk stratification.
Language	English
Publishing date	2022-08-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3040546-4
ISSN	2666-1683 ; 2058-4881
ISSN (online)	2666-1683
ISSN	2058-4881
DOI	10.1016/j.euros.2022.07.004
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Article: Ephrin B Activate Src Family Kinases in Fibroblasts Inducing Stromal Remodeling in Prostate Cancer.

Kakarla, Mamatha / ChallaSivaKanaka, Sathyavathi / Dufficy, Mary F / Gil, Victoria / Filipovich, Yana / Vickman, Renee / Crawford, Susan E / Hayward, Simon W / Franco, Omar E

Cancers

2022 Volume 14, Issue 9

Abstract: Through stromal-epithelial interactions, carcinoma associated fibroblasts (CAF) play a critical role in tumor growth and progression. Activation of erythrophoyetin-producing human hepatocellular (Eph) receptors has been implicated in cancer. Eph receptor ...

Abstract	Through stromal-epithelial interactions, carcinoma associated fibroblasts (CAF) play a critical role in tumor growth and progression. Activation of erythrophoyetin-producing human hepatocellular (Eph) receptors has been implicated in cancer. Eph receptor interactions with Ephrin ligands lead to bidirectional signals in the recipient and effector cells. The consequences of continuous reverse Ephrin signaling activation in fibroblasts on prostate cancer (PCa) is unknown. When compared to benign prostate fibroblast, CAF displayed higher expression of Ephrin B1, B2, and B3 ligands (EFNB1, EFNB2, and EFNB3). In this study, we found that continuous activation of EFNB1 and EFNB3 in a benign human prostate stromal cell line (BHPrS1) increased the expression of CAF markers and induced a CAF phenotype. BHPrS1
Language	English
Publishing date	2022-05-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14092336
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Article: Vascular interference: a blockade to tumor epithelial growth.

Crawford, Susan E

Hepatology (Baltimore, Md.)

2004 Volume 39, Issue 6, Page(s) 1491–1494

MeSH term(s)	Animals ; Humans ; Liver/pathology ; Liver Neoplasms/pathology ; Liver Neoplasms/prevention & control ; Liver Regeneration/physiology ; Neovascularization, Physiologic ; Vascular Endothelial Growth Factor A/antagonists & inhibitors ; Vascular Endothelial Growth Factor A/physiology
Chemical Substances	Vascular Endothelial Growth Factor A
Language	English
Publishing date	2004-06
Publishing country	United States
Document type	Comment ; Journal Article ; Review
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.20278
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Zs.A 1660: Show issues

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Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: PEDF deficiency increases the susceptibility of rd10 mice to retinal degeneration.

Dixit, Shivani / Polato, Federica / Samardzija, Marijana / Abu-Asab, Mones / Grimm, Christian / Crawford, Susan E / Becerra, S Patricia

Experimental eye research

2020 Volume 198, Page(s) 108121

Abstract: The SERPINF1 gene encodes pigment epithelium-derived factor (PEDF), a member of the serpin superfamily with neurotrophic and antiangiogenic properties in the retina. We hypothesized that absence of PEDF would lead to increased stress-associated retinal ... ...

Abstract	The SERPINF1 gene encodes pigment epithelium-derived factor (PEDF), a member of the serpin superfamily with neurotrophic and antiangiogenic properties in the retina. We hypothesized that absence of PEDF would lead to increased stress-associated retinal degeneration in Serpinf1 null mice. Accordingly, using a Serpinf1 null mouse model, we investigated the impact of PEDF absence on retinal morphology, and susceptibility to induced and inherited retinal degeneration. We studied the pattern of Serpinf1 expression in the mouse retina layers. PEDF protein was detected by western blotting. Transmission electron microscopy was performed on mouse retina. Serpinf1 null mice and wild type littermates were injected with NaIO
MeSH term(s)	Animals ; Blotting, Western ; Disease Models, Animal ; Disease Progression ; Eye Proteins/genetics ; Eye Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Growth Factors/deficiency ; Nerve Growth Factors/genetics ; Nerve Growth Factors/metabolism ; Photoreceptor Cells, Vertebrate/metabolism ; Photoreceptor Cells, Vertebrate/pathology ; Retinal Degeneration/metabolism ; Retinal Degeneration/pathology ; Retinal Pigment Epithelium/metabolism ; Retinal Pigment Epithelium/pathology ; Serpins/deficiency ; Serpins/genetics ; Serpins/metabolism
Chemical Substances	Eye Proteins ; Nerve Growth Factors ; Serpins ; pigment epithelium-derived factor
Language	English
Publishing date	2020-07-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80122-7
ISSN	1096-0007 ; 0014-4835
ISSN (online)	1096-0007
ISSN	0014-4835
DOI	10.1016/j.exer.2020.108121
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Zs.A 163: Show issues

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ab Jg. 2022: Lesesaal (EG)

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Article ; Online: DGAT1 Inhibitor Suppresses Prostate Tumor Growth and Migration by Regulating Intracellular Lipids and Non-Centrosomal MTOC Protein GM130.

Nardi, Francesca / Franco, Omar E / Fitchev, Philip / Morales, Alejandro / Vickman, Renee E / Hayward, Simon W / Crawford, Susan E

Scientific reports

2019 Volume 9, Issue 1, Page(s) 3035

Abstract: Acyl-CoA:diacylglycerol acyltransferase I (DGAT1) is a key enzyme in lipogenesis which is increased in metabolically active cells to meet nutrient requirements. DGAT1 has been recognized as an anti-obesity target; however, its role in the tumor ... ...

Abstract	Acyl-CoA:diacylglycerol acyltransferase I (DGAT1) is a key enzyme in lipogenesis which is increased in metabolically active cells to meet nutrient requirements. DGAT1 has been recognized as an anti-obesity target; however, its role in the tumor microenvironment remains unclear. We postulated that, in prostate cancer (PCa) cells, augmented lipogenesis and growth are due to increased DGAT1 expression leading to microtubule-organizing center (MTOC) amplification. Thus, therapeutic targeting of DGAT1 potentially has tumor suppressive activity. We tested whether blocking DGAT1 in PCa cells altered MTOC and lipid signaling. Western blot and immunofluorescence were performed for MTOC and triglyceride mediators. Treatment with a DGAT1 inhibitor was evaluated. We found a stepwise increase in DGAT1 protein levels when comparing normal prostate epithelial cells to PCa cells, LNCaP and PC-3. Lipid droplets, MTOCs, and microtubule-regulating proteins were reduced in tumor cells treated with a DGAT1 inhibitor. Depletion of the non-centrosomal MTOC protein GM130 reduced PCa cell proliferation and migration. Inhibition of DGAT1 reduced tumor growth both in vitro and in vivo, and a negative feedback loop was discovered between DGAT1, PEDF, and GM130. These data identify DGAT1 as a promising new target for suppressing PCa growth by regulating GM130, MTOC number and disrupting microtubule integrity.
MeSH term(s)	Autoantigens/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Movement/physiology ; Cell Proliferation/physiology ; Diacylglycerol O-Acyltransferase/metabolism ; Epithelial Cells/metabolism ; Eye Proteins/metabolism ; Humans ; Lipid Droplets/metabolism ; Lipids ; Lipogenesis/physiology ; Male ; Membrane Proteins/metabolism ; Microtubule-Organizing Center/metabolism ; Microtubules/metabolism ; Nerve Growth Factors/metabolism ; PC-3 Cells ; Prostate/metabolism ; Prostatic Neoplasms/metabolism ; Serpins/metabolism
Chemical Substances	Autoantigens ; Eye Proteins ; Golgin subfamily A member 2 ; Lipids ; Membrane Proteins ; Nerve Growth Factors ; Serpins ; pigment epithelium-derived factor ; DGAT1 protein, human (EC 2.3.1.20) ; Diacylglycerol O-Acyltransferase (EC 2.3.1.20)
Language	English
Publishing date	2019-02-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-39537-z
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