{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T10:44:25Z","timestamp":1790419465907,"version":"4.1.0"},"reference-count":59,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","funder":[{"DOI":"10.13039\/100003925","name":"Lowe Syndrome Association","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100003925","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 DK101484"],"award-info":[{"award-number":["R01 DK101484"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 DK118726"],"award-info":[{"award-number":["R01 DK118726"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["S10 OD021627"],"award-info":[{"award-number":["S10 OD021627"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Pittsburgh Center for Kidney Research","award":["P30 DK079307"],"award-info":[{"award-number":["P30 DK079307"]}]},{"name":"Pittsburgh Center for Kidney Research","award":["T32 DK061296"],"award-info":[{"award-number":["T32 DK061296"]}]},{"name":"Pittsburgh Center for Kidney Research","award":["TL1 TR001858"],"award-info":[{"award-number":["TL1 TR001858"]}]},{"name":"Pittsburgh Center for Kidney Research","award":["T32 DK061296"],"award-info":[{"award-number":["T32 DK061296"]}]},{"DOI":"10.13039\/100001463","name":"American Society of Nephrology","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001463","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"NIH","doi-asserted-by":"publisher","award":["F31 DK121394"],"award-info":[{"award-number":["F31 DK121394"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"NIH","doi-asserted-by":"publisher","award":["R01 DK103645"],"award-info":[{"award-number":["R01 DK103645"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2020,1]]},"abstract":"\n Significance Statement<\/jats:title>\n \n Patients with Lowe syndrome (LS) develop abnormalities in proximal tubule function that cause declining kidney function. Mutations in the\n OCRL<\/jats:italic>\n gene encoding cause LS. The enzyme encoded by\n OCRL<\/jats:italic>\n hydrolyzes phosphatidylinositol 4,5-bisphosphate, a lipid that regulates myriad cellular functions. The authors created a knockout model of OCRL in human proximal tubule cells and observed that loss of OCRL impairs cell proliferation and results in the accumulation of multinucleated cells.\n Lrp2<\/jats:italic>\n -positive segments of the pronephric kidney were shorter in\n ocrl<\/jats:italic>\n mutant and morphant zebrafish. The authors also created a mathematic model that explains how loss of functional OCRL can lead to the kidney manifestations of LS. The authors hypothesize that impaired cell proliferation results in a shorter proximal tubule in patients with LS and that this contributes to proteinuria.\n <\/jats:p>\n <\/jats:sec>\n \n Background<\/jats:title>\n \n Lowe syndrome (LS) is an X-linked recessive disorder caused by mutations in\n OCRL<\/jats:italic>\n , which encodes the enzyme OCRL. Symptoms of LS include proximal tubule (PT) dysfunction typically characterized by low molecular weight proteinuria, renal tubular acidosis (RTA), aminoaciduria, and hypercalciuria. How mutant\n OCRL<\/jats:italic>\n causes these symptoms isn\u2019t clear.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n We examined the effect of deleting OCRL on endocytic traffic and cell division in newly created human PT CRISPR\/Cas9\n OCRL<\/jats:italic>\n knockout cells, multiple PT cell lines treated with\n OCRL<\/jats:italic>\n -targeting siRNA, and in\n orcl<\/jats:italic>\n -mutant zebrafish.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n OCRL-depleted human cells proliferated more slowly and about 10% of them were multinucleated compared with fewer than 2% of matched control cells. Heterologous expression of wild-type, but not phosphatase-deficient, OCRL prevented the accumulation of multinucleated cells after acute knockdown of OCRL but could not rescue the phenotype in stably edited knockout cell lines. Mathematic modeling confirmed that reduced PT length can account for the urinary excretion profile in LS. Both\n ocrl<\/jats:italic>\n mutant zebrafish and zebrafish injected with\n ocrl<\/jats:italic>\n morpholino showed truncated expression of megalin along the pronephric kidney, consistent with a shortened S1 segment.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n Our data suggest a unifying model to explain how loss of OCRL results in tubular proteinuria as well as the other commonly observed renal manifestations of LS. We hypothesize that defective cell division during kidney development and\/or repair compromises PT length and impairs kidney function in LS patients.<\/jats:p>\n <\/jats:sec>","DOI":"10.1681\/asn.2019020125","type":"journal-article","created":{"date-parts":[[2019,11,1]],"date-time":"2019-11-01T16:05:23Z","timestamp":1572624323000},"page":"67-83","source":"Crossref","is-referenced-by-count":21,"title":["Effects of Proximal Tubule Shortening on Protein Excretion in a Lowe Syndrome Model"],"prefix":"10.1681","volume":"31","author":[{"given":"Megan L.","family":"Gliozzi","sequence":"first","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eugenel B.","family":"Espiritu","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katherine 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Pittsburgh Liver Research Center, Pittsburgh, Pennsylvania;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew J.","family":"Lazzara","sequence":"additional","affiliation":[{"name":"Department of Chemical Engineering, University of Virginia, Charlottesville, Virginia; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neil A.","family":"Hukriede","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, and"},{"name":"Center for Critical Care Nephrology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine J.","family":"Baty","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ora A.","family":"Weisz","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of 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