Lymphatic Vasculature Requires Estrogen Receptor-α Signaling to Protect From Lymphedema

Morfoisse, Florent; Tatin, Florence; Chaput, Benoît; Therville, Nicole; Vaysse, Charlotte; Métivier, Raphaël; Malloizel‐Delaunay, Julie; Pujol, Françoise; Godet, Anne-Claire; Toni, Fabienne de; Boudou, Frédéric; Grenier, Katia; Dubuc, David; Lacazette, Éric; Prats, Anne-Catherine; Guillermet-Guibert, Julie; Lenfant, Françoise; Garmy‐Susini, Barbara

doi:10.1161/atvbaha.118.310997

Cited by 47 publications

(64 citation statements)

References 43 publications

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“…They identified the estrogen receptor α (ERα) as a key player of the lymphatic endothelial function. In agreement with these findings, they highlighted the detrimental role of hormone therapy on the lymphatic system leading to an aggravation of lymphedema [4]. …”

supporting

confidence: 70%

Hormone therapy outcome in lymphedema

Garmy‐Susini

2019

Aging

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supporting

confidence: 70%

Hormone therapy outcome in lymphedema

Garmy‐Susini

2019

Aging

Self Cite

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“…In addition to its promotion of amyloid-β removal potentially through stimulating IPAD, taxifolin elevated the expression levels of the lymphangiogenic factors LYVE-1 and VEGF-D. Central VEGF-D is necessary for neuronal function and cognition (48), so our findings imply that taxifolin has beneficially affected cognitive function as well as the integrity of the lymphatic vasculature. The mechanisms underlying the taxifolinmediated up-regulation of LYVE-1 and VEGF-D remain unclear; however, a recent study reported that these factors were expressed by estrogen receptor signaling, thereby increasing skin lymphangiogenesis (49). In addition, the estrogen receptor has been reported to function as a receptor for taxifolin (50).…”

Section: Discussionmentioning

confidence: 99%

Pleiotropic neuroprotective effects of taxifolin in cerebral amyloid angiopathy

Inoue

Saitô

Tanaka

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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Cerebral amyloid angiopathy (CAA) results from amyloid-β deposition in the cerebrovasculature. It is frequently accompanied by Alzheimer's disease and causes dementia. We recently demonstrated that in a mouse model of CAA, taxifolin improved cerebral blood flow, promoted amyloid-β removal from the brain, and prevented cognitive dysfunction when administered orally. Here we showed that taxifolin inhibited the intracerebral production of amyloid-β through suppressing the ApoE-ERK1/2-amyloid-β precursor protein axis, despite the low permeability of the bloodbrain barrier to taxifolin. Higher expression levels of triggering receptor expressed on myeloid cell 2 (TREM2) were associated with the exacerbation of inflammation in the brain. Taxifolin suppressed inflammation, alleviating the accumulation of TREM2expressing cells in the brain. It also mitigated glutamate levels and oxidative tissue damage and reduced brain levels of active caspases, indicative of apoptotic cell death. Thus, the oral administration of taxifolin had intracerebral pleiotropic neuroprotective effects on CAA through suppressing amyloid-β production and beneficially modulating proinflammatory microglial phenotypes.cerebral amyloid angiopathy | neuroprotection | taxifolin | triggering receptor expressed on myeloid cell 2

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“…Such lymphatic dysfunction can occur prior to treatments of surgical dissection and/or RT, suggesting that cancer progression, particularly LN metastasis, contributes to lymphatic dysfunction in cancer patients prior to surgery and RT. While there is evidence that chemotherapy may potentially contribute to the development of cancer-acquired LE [66][67][68][69], further longitudinal studies are needed to understand all the contributing factors that can cause lymphatic dysfunction. Nonetheless, recent results in Figure 7 confirm the results of other studies showing subclinical edema measured with bioimpedance of water content in the arms in breast cancer patients prior to first-line treatment [70,71].…”

Section: The Effects Of Metastasis and Cancer Progression On Lymphatimentioning

confidence: 99%

The Development and Treatment of Lymphatic Dysfunction in Cancer Patients and Survivors

Aldrich

Rasmussen

Fife

et al. 2020

Cancers

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Breast-cancer-acquired lymphedema is routinely diagnosed from the appearance of irreversible swelling that occurs as a result of lymphatic dysfunction. Yet in head and neck cancer survivors, lymphatic dysfunction may not always result in clinically overt swelling, but instead contribute to debilitating functional outcomes. In this review, we describe how cancer metastasis, lymph node dissection, and radiation therapy alter lymphatic function, as visualized by near-infrared fluorescence lymphatic imaging. Using custom gallium arsenide (GaAs)-intensified systems capable of detecting trace amounts of indocyanine green administered repeatedly as lymphatic contrast for longitudinal clinical imaging, we show that lymphatic dysfunction occurs with cancer progression and treatment and is an early, sub-clinical indicator of cancer-acquired lymphedema. We show that early treatment of lymphedema can restore lymphatic function in breast cancer and head and neck cancer patients and survivors. The compilation of these studies provides insights to the critical role that the lymphatics and the immune system play in the etiology of lymphedema and associated co-morbidities.

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Lymphatic Vasculature Requires Estrogen Receptor-α Signaling to Protect From Lymphedema

Cited by 47 publications

References 43 publications

Hormone therapy outcome in lymphedema

Hormone therapy outcome in lymphedema

Pleiotropic neuroprotective effects of taxifolin in cerebral amyloid angiopathy

The Development and Treatment of Lymphatic Dysfunction in Cancer Patients and Survivors

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