Hyperplasia, de novo lymphangiogenesis, and lymphatic regression in mice with tissue-specific, inducible overexpression of murine VEGF-D

Lammoglia, Gabriela M.; Zandt, Carolynn E. Van; Galvan, Daniel X.; Orozco, Jose L.; Dellinger, Michael T.; Rutkowski, Joseph M.

doi:10.1152/ajpheart.00208.2016

Cited by 34 publications

(40 citation statements)

References 57 publications

(67 reference statements)

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“…However, rapid spontaneous regression of lymphatics has been reported in corneal inflammation (48), mammary gland regression after lactation (49), lymph node involution (50), adipose tissue after stopping VEGF-D overexpression (51), and intestinal lacteals after genetic deletion of VEGF-C (46). Further studies are needed to learn the mechanisms underlying the differences in dependence of lymphatics on environment survival factors.…”

Section: Attributes and Limitations Of The Ccsp/vegf-c Mouse Model Ofmentioning

confidence: 99%

Rapamycin reversal of VEGF-C–driven lymphatic anomalies in the respiratory tract

Bałuk¹,

Yao²,

Flores³

et al. 2017

JCI Insight

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Section: Attributes and Limitations Of The Ccsp/vegf-c Mouse Model Ofmentioning

confidence: 99%

Rapamycin reversal of VEGF-C–driven lymphatic anomalies in the respiratory tract

Bałuk¹,

Yao²,

Flores³

et al. 2017

JCI Insight

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“…However, overexpression of VEGF-D can induce lymphangiogenesis and angiogenesis under normal and pathological conditions (Baldwin et al, 2005;Bui et al, 2016). Overexpression of VEGF-D in lungs, kidneys, and adipose tissue induces hyperplasia of lymphatic vessels and lymphangiectasia (Lammoglia et al, 2016). Moreover, longterm overexpression of VEGF-D in adipose tissue of mice caused increased macrophage infiltration and enhanced adipose tissue fibrosis (Lammoglia et al, 2016).…”

Section: Vegf-c Vegf-d and Vegfr3mentioning

confidence: 99%

“…Overexpression of VEGF-D in lungs, kidneys, and adipose tissue induces hyperplasia of lymphatic vessels and lymphangiectasia (Lammoglia et al, 2016). Moreover, longterm overexpression of VEGF-D in adipose tissue of mice caused increased macrophage infiltration and enhanced adipose tissue fibrosis (Lammoglia et al, 2016). However, overexpression VEGF-D did not result in obesity or insulin resistance in chow diet fed mice (Lammoglia et al, 2016).…”

Section: Vegf-c Vegf-d and Vegfr3mentioning

confidence: 99%

“…Moreover, longterm overexpression of VEGF-D in adipose tissue of mice caused increased macrophage infiltration and enhanced adipose tissue fibrosis (Lammoglia et al, 2016). However, overexpression VEGF-D did not result in obesity or insulin resistance in chow diet fed mice (Lammoglia et al, 2016). Surprisingly, in high-fat diet fed condition overexpression of VEGF-D in the adipocytes resulted in enhanced glucose clearance, lower insulin levels and reduced liver triglycerides (Chakraborty et al, 2019).…”

Section: Vegf-c Vegf-d and Vegfr3mentioning

confidence: 99%

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Lymphatic Vasculature in Energy Homeostasis and Obesity

Srinivasan

2020

Front. Physiol.

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Obesity is a leading cause of cardiovascular diseases and cancer. Body mass is regulated by the balance between energy uptake and energy expenditure. The etiology of obesity is determined by multiple factors including genetics, nutrient absorption, and inflammation. Lymphatic vasculature is starting to be appreciated as a critical modulator of metabolism and obesity. The primary function of lymphatic vasculature is to maintain interstitial fluid homeostasis. Lymphatic vessels absorb fluids that extravasate from blood vessels and return them to blood circulation. In addition, lymphatic vessels absorb digested lipids from the intestine and regulate inflammation. Hence, lymphatic vessels could be an exciting target for treating obesity. In this article, we will review our current understanding regarding the relationship between lymphatic vasculature and obesity, and highlight some open questions.

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“…124 Recently, we developed a mouse model with inducible adipocyte-specific overexpression of VEGF-D and, while the mice demonstrated a massive ....................................................................................................................... expansion of lymphatic networks in adipose tissues, macrophage recruitment and inflammation were also increased. 107 With high fat diet feeding that normally drives adipose tissue inflammation, fewer resident macrophages were found with increased lymphatic density (Figure 2). Uncoupling the negative chemokine aspects of these lymphatic growth factors from the potentially positive effects of increased lymphatic density is currently underway.…”

Section: Lymphangiogenesis and Renal Diseasementioning

confidence: 99%

Lymphangiogenesis: fuel, smoke, or extinguisher of inflammation’s fire?

Abouelkheir

Upchurch

Rutkowski

2017

Exp Biol Med (Maywood)

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Lymphangiogenesis is a recognized hallmark of inflammatory processes in tissues and organs as diverse as the skin, heart, bowel, and airways. In clinical and animal models wherein the signaling processes of lymphangiogenesis are manipulated, most studies demonstrate that an expanded lymphatic vasculature is necessary for the resolution of inflammation. The fundamental roles that lymphatics play in fluid clearance and immune cell trafficking from the periphery make these results seemingly obvious as a mechanism of alleviating locally inflamed environments: the lymphatics are simply providing a drain. Depending on the tissue site, lymphangiogenic mechanism, or induction timeframe, however, evidence shows that inflammation-associated lymphangiogenesis (IAL) may worsen the pathology. Recent studies have identified lymphatic endothelial cells themselves to be local regulators of immune cell activity and its consequential phenotypes – a more active role in inflammation regulation than previously thought. Indeed, results focusing on the immunocentric roles of peripheral lymphatic function have revealed that the basic drainage task of lymphatic vessels is a complex balance of locally processed and transported antigens as well as interstitial cytokine and immune cell signaling: an interplay that likely defines the function of IAL. This review will summarize the latest findings on how IAL impacts a series of disease states in various tissues in both preclinical models and clinical studies. This discussion will serve to highlight some emerging areas of lymphatic research in an attempt to answer the question relevant to an array of scientists and clinicians of whether IAL helps to fuel or extinguish inflammation. Impact statement Inflammatory progression is present in acute and chronic tissue pathologies throughout the body. Lymphatic vessels play physiological roles relevant to all medical fields as important regulators of fluid balance, immune cell trafficking, and immune identity. Lymphangiogenesis is often concurrent with inflammation and can potentially aide or worsen disease progression. How new lymphatic vessels impact inflammation and by which mechanism is an important consideration in current and future clinical therapies targeting inflammation and/or vasculogenesis. This review identifies, across a range of tissue-specific pathologies, the current understanding of inflammation-associated lymphangiogenesis in the progression or resolution of inflammation.

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Hyperplasia, de novo lymphangiogenesis, and lymphatic regression in mice with tissue-specific, inducible overexpression of murine VEGF-D

Abstract: Lammoglia GM, Van Zandt CE, Galvan DX, Orozco JL, Dellinger MT, Rutkowski JM. Hyperplasia, de novo lymphangiogenesis, and lymphatic regression in mice with tissue-specific, inducible overexpression of murine VEGF-D.

Cited by 34 publications

References 57 publications

Rapamycin reversal of VEGF-C–driven lymphatic anomalies in the respiratory tract

Rapamycin reversal of VEGF-C–driven lymphatic anomalies in the respiratory tract

Lymphatic Vasculature in Energy Homeostasis and Obesity

Lymphangiogenesis: fuel, smoke, or extinguisher of inflammation’s fire?

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