scholarly journals Postnatal Growth Restriction in Mice Alters Cardiac Protein Composition and Leads to Functional Impairment in Adulthood

2020 ◽  
Vol 21 (24) ◽  
pp. 9459
Author(s):  
Joseph R. Visker ◽  
Lawrence J. Dangott ◽  
Eric C. Leszczynski ◽  
David P. Ferguson
Keyword(s):  
Cardiac Function ◽  
Western Blotting ◽  
Leukemia Virus ◽  
Protein Composition ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Western Blots ◽  
2D Dige ◽  
Friend Leukemia ◽  
Silver Nitrate Staining

Postnatal growth restriction (PGR) increases the risk for cardiovascular disease (CVD) in adulthood, yet there is minimal mechanistic rationale for the observed pathology. The purpose of this study was to identify proteomic differences in hearts of growth-restricted and unrestricted mice, and propose mechanisms related to impairment in adulthood. Friend leukemia virus B (FVB) mouse dams were fed a control (CON: 20% protein), or low-protein (LP: 8% protein) isocaloric diet 2 weeks before mating. LP dams produce 20% less milk, inducing growth restriction. At birth (postnatal; PN1), pups born to dams fed the CON diet were switched to LP dams (PGR group) or a different CON dam. At PN21, a sub-cohort of CON (n = 3 males; n = 3 females) and PGR (n = 3 males; n = 3 females) were euthanized and their proteome analyzed by two-dimensional differential in-gel electrophoresis (2D DIGE) and mass spectroscopy. Western blotting and silver nitrate staining confirmed 2D DIGE results. Littermates (CON: n = 4 males and n = 4 females; PGR: n = 4 males and n = 4 females) were weaned to the CON diet. At PN77, echocardiography measured cardiac function. At PN80, hearts were removed for western blotting to determine if differences persisted into adulthood. 2D DIGE and western blot confirmation indicated PGR had reductions in p57kip2, Titin (Ttn), and Collagen (Col). At PN77, PGR had impaired cardiac function as measured by echocardiography. At PN80, western blots of p57kip2 showed protein abundance recovered from PN21. PN80 silver staining of large molecular weight proteins (Ttn and Col) was reduced in PGR. PGR reduces cell cycle activity at PN21, which is recovered in adulthood. However, collagen fiber networks are altered into adulthood.

When early life growth restriction in rats is followed by attenuated postnatal growth: effects on cardiac function in adulthood

2014 ◽  
Vol 54 (5) ◽  
pp. 743-750 ◽  
Author(s):  
Vladislava Zohdi ◽  
James T. Pearson ◽  
Michelle M. Kett ◽  
Paul Lombardo ◽  
Michal Schneider ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Early Life ◽  
Postnatal Growth ◽  
Growth Restriction ◽  
Growth Effects

Recent Studies on a Murine Leukemia Virus Grown in Tissue Culture

1967 ◽  
Vol 25 ◽  
pp. 106-107
Author(s):  
L. Z. de Tkaczevski ◽  
E. de Harven ◽  
C. Friend
Keyword(s):  
Tissue Culture ◽  
Solid Tumors ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Supernatant Fluid ◽  
Virus Particles ◽  
Friend Leukemia ◽  
Type C ◽  
Leukemia Viruses ◽  
Murine Leukemia

Despite extensive studies, the correlation between the morphology and pathogenicity of murine leukemia viruses (MLV) has not yet been clarified. The virus particles found in the plasma of leukemic mice belong to 2 distinct groups, 1 or 2% of them being enveloped A particles and the vast majority being of type C. It is generally believed that these 2 types of particles represent different phases in the development of the same virus. Particles of type A have been thought to be an earlier form of type C particles. One of the tissue culture lines established from Friend leukemia solid tumors has provided the material for the present study. The supernatant fluid of the line designated C-1A contains an almost pure population of A particles as illustrated in Figure 1. The ratio is, therefore, the reverse of what is unvariably observed in the plasma of leukemic mice where C particles predominate.

Involvement of GER in Friend leukemia virus assembly in high-pressure frozen cells

1990 ◽  
Vol 48 (3) ◽  
pp. 590-591
Author(s):  
W. Djaczenko ◽  
M. Müller ◽  
A. Benedetto ◽  
G. Carbone
Keyword(s):  
High Pressure ◽  
Virus Assembly ◽  
Leukemia Virus ◽  
Leukemia Cells ◽  
Serial Sections ◽  
Myeloma Cells ◽  
Virus Particles ◽  
Friend Leukemia ◽  
Carbon Coated ◽  
Friend Leukemia Virus

A thickening of ER membranes in murine myeloma cells was attributed by de Harven to the assembly of intracisternal virus particles. We observed similar thickening of GER membranes in Friend leukemia cells (FLC) apparently associated with Friend leukemia virus (FLV) assembly. We reinvestigated the problem of GER involvement in FLV assembly using high pressure cryofixed FLC.FLC (745A clone growing in suspension and FF clone growing in monolayer) were immersed in Hexadecene (Fluka, Switzerland) and rapidly frozen in Balzers HPM 010 freezing machine working at 2200 bar. All cells were freeze substituted at -90°C in 2% OsO4 in absolute acetone. Serial sections cut to avoid misinterpretations due to the geometry of sections, were collected on carbon coated 100 mesh grids.

Abstract 269: Miofibroblast Tgf-beta Signaling in a Proteotoxic Mouse Model

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Bidur Bhandary ◽  
Qinghang Meng ◽  
Hanna Osinska ◽  
Kritton Shay-Winkler ◽  
James Gulick ◽  
...  
Keyword(s):  
Heart Disease ◽  
Mouse Model ◽  
Cardiac Function ◽  
Transforming Growth Factor Beta ◽  
Cardiac Fibrosis ◽  
Transforming Growth Factor ◽  
Prolonged Survival ◽  
Tgfβ Signaling ◽  
Specific Expression ◽  
Western Blots

Introduction: Transforming Growth Factor Beta (TGFβ) is an important cytokine in mediating the fibrogenic response and, in particular, cardiac fibrosis. Extensive fibrosis accompanies the cardiac remodeling that occurs during development of the protein conformation-based disease caused by cardiomyocyte-specific expression of a mutant, small, heat shock-like protein and chaperone, aB crystallin (CryABR120G). During the onset of fibrosis, fibroblasts are activated to the so-called “myofibroblast” state and TGFβ binding is thought to mediate an essential signaling pathway underlying this process. Our central hypothesis is that TGFβ signaling processes that result in significant cardiac fibrosis in a mouse model of proteotoxic heart disease are mediated by cardiac fibroblasts, rather than cardiomyocytes. Here, we have partially ablated TGFβ signaling only in cardiac myofibroblasts to observe if cardiac fibrosis is reduced. Aims and Methods: The objective of this study was to understand the contributions of fibroblast-derived TGFβ signaling to the development of cardiac fibrosis in a proteotoxic mouse model that results in significant cardiac fibrosis. To test the hypothesis we partially deleted the myofibroblast specific canonical and non-canonical signaling by crossing CryAB R120G mice with Tgfbr1 or Tgfbr2 floxed mice. The double transgene containing mice were further crossed with activated myofibroblast specific Cre mice in which Cre expression was driven off the periostin promoter. Echocardiography, Masson’s Trichome staining, PCR arrays, IHC and western blots were performed to characterize the fibrotic progression in CryAB R120G transgenic mice. Results: We observed that myofibroblast-targeted partial knockdown of Tgf βr1 signaling prolonged survival, modestly reducing fibrosis and improving cardiac function . Similarly, Tgf βr2 partial knockdown prolonged survival, modestly reducing fibrosis without improving cardiac function during fibrosis development in CryAB R120G mice. Conclusion: These findings suggest that, in a model of proteotoxic heart disease, myofibroblast based TGFβ signaling in the heart may contribute to cardiac hypertrophy/dysfunction but cannot account entirely for the fibrotic response.

What can we learn from Fli1-deficient mice, new animal models of systemic sclerosis?

2018 ◽  
Vol 3 (1) ◽  
pp. 6-13 ◽  
Author(s):  
Yoshihide Asano
Keyword(s):  
Systemic Sclerosis ◽  
Animal Models ◽  
Leukemia Virus ◽  
Environmental Influences ◽  
Epidemiological Studies ◽  
Potential Candidate ◽  
Predisposing Factor ◽  
Friend Leukemia ◽  
Virus Integration ◽  
Friend Leukemia Virus

Systemic sclerosis is a complex multifactorial disease characterized by autoimmunity, vasculopathy, and selective organ fibrosis. A series of genetic and epidemiological studies have demonstrated that environmental influences play a central role in the onset of systemic sclerosis, while genetic factors determine the susceptibility to and the severity of this disease. Therefore, the identification of predisposing factors related to environmental influences would provide us with an informative clue to better understand the pathological process of this disease. Based on this concept, the deficiency of transcription factor Friend leukemia virus integration 1, which is epigenetically suppressed in systemic sclerosis, seems to be a potential candidate acting as the predisposing factor of this disease. Indeed, Fli1-mutated mice serve as a set of useful disease models to disclose the complex pathology of systemic sclerosis. This article overviews the recent advancement in systemic sclerosis animal models associated with Friend leukemia virus integration 1 deficiency.

Somatic growth and the risks of bronchopulmonary dysplasia and pulmonary hypertension: connecting epidemiology and physiology

2019 ◽  
Vol 97 (3) ◽  
pp. 197-205 ◽  
Author(s):  
Mark A. Underwood ◽  
Stephen Wedgwood ◽  
Satyan Lakshminrusimha ◽  
Robin H. Steinhorn
Keyword(s):  
Pulmonary Hypertension ◽  
Bronchopulmonary Dysplasia ◽  
Somatic Growth ◽  
Postnatal Growth ◽  
Pulmonary Complications ◽  
Growth Restriction ◽  
Extreme Prematurity ◽  
Poor Growth ◽  
Increased Risk ◽  
Poor Nutrition

In the premature infant, poor growth in utero (fetal growth restriction) and in the first weeks of life (postnatal growth restriction) are associated with increased risk for bronchopulmonary dysplasia and pulmonary hypertension. In this review, we summarize the epidemiologic data supporting these associations, present a novel rodent model of postnatal growth restriction, and review 5 promising mechanisms by which poor nutrition may affect the developing lung. These observations support the hypothesis that nutritional and (or) pharmacologic interventions early in life may be able to decrease risk of the pulmonary complications of extreme prematurity.

Maternal cardiac function in normotensive and pre-eclamptic intrauterine growth restriction

2008 ◽  
Vol 32 (5) ◽  
pp. 682-686 ◽  
Author(s):  
J. E. A. K. Bamfo ◽  
N. A. Kametas ◽  
J. B. Chambers ◽  
K. H. Nicolaides
Keyword(s):  
Cardiac Function ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth
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