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Absence of Mast Cells in the Kidneys of Rats Subjected to Fat Embolism Despite their Presence in the Lungs and Heart
Author(s) -
Patel Chirag,
Fletcher Amanda N,
Poisner Alan M,
Siddiqi Ahsan,
Arif Dauod,
Hamidpour Soheila,
Ponnapureddy Rakesh,
Molteni Agostino
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.445.1
Subject(s) - fibrosis , trichrome stain , medicine , renin–angiotensin system , endocrinology , kidney , saline , losartan , angiotensin ii , pathology , receptor , blood pressure , immunohistochemistry
In a rat model of fat embolism (FE) induced by i.v. injection of triolein (T), we have shown that the lungs, hearts and kidneys demonstrate severe histopathological damage characterized by organ inflammation and arterial constriction. 1,2,3 Such damage is present up to 10 weeks after injection.1 The renin angiotensin system (RAS) plays a role in the pathogenesis of the damage since captopril (an ACE inhibitor) and losartan (Los), an angiotensin‐II type 1 receptor blocker, prevented the damage.4 After T injection, an increase in renin stain was observed in the kidney juxta‐glomerular apparatus (JXTG)5 and in the lungs.6 The renin overexpression may be related to an increased number of mast cells (MCs),7 and indeed we found an increased number of these cells 10 weeks post T injection in the lungs of the rats.8 MCs in lower numbers were also observed in hearts of the same rats, but LOS did not reduce their number.9 On the basis of these observations, we decided to evaluate the potential presence of MCs in kidneys after T injection. Twenty‐two Sprague Dawley rats (~300 gm BW) received either T (0.2 mL i.v.) or saline. Six weeks later, half of the rats were given i.p. injection of Los and the remainder received saline. Four weeks later (10 weeks post T injection), rats were anesthetized with isoflurane, sacrificed, and necropsied. Tissues were fixed in 10% formalin and stained with H&E (morphometric scoring), Trichrome (fibrosis) and CD 11‐c kit (MCs). On each slide, 10 photographs were taken at random at 400× and MCs evaluated by two pathologists unaware of the slide identity. After T injection, we observed severe arterial damage with increased medial thickness and reduced lumen patency. Glomeruli showed increased cellularity, thickening of basal membrane, and crescent formation. Scattered chronic inflammatory cells and erythrocytes were seen in the tubuli. The damage was moderately reduced by Los treatment. MCs were not seen in any of the animals. In the kidneys, despite the high presence of renin in the JXTG and severe vasculitis after T injection, we could not identify MCs at 10 weeks even with a very specific staining method. This is in contrast with the presence of MCs that we have found in the lungs and heart. The absence of MCs in the kidneys at 10 weeks may reflect different pathogenic mechanisms or a time course different from that of the lungs or heart. Support or Funding Information M. K. Geldmacher Foundation, St. Louis, MO; This work was supported by a CTSA grant from NCRR and NCATS awarded to the University of Kansas Medical Center for Frontiers: The Heartland Institute for Clinical and Translational Research # TL1TR000120. The contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH, NCRR, or NCATS.