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  • 101. Zhang, Wenjing
    et al.
    Dai, Min
    Fridberger, Anders
    Karolinska Institutet, Stockholm, Sweden.
    Hassan, Ahmed
    Degagne, Jacqueline
    Neng, Lingling
    Zhang, Fei
    He, Wenxuan
    Ren, Tianying
    Trune, Dennis
    Auer, Manfred
    Shi, Xiaorui
    Perivascular-resident macrophage-like melanocytes in the inner ear are essential for the integrity of the intrastrial fluid-blood barrier2012Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 109, nr 26, s. 10388-10393Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The microenvironment of the cochlea is maintained by the barrier between the systemic circulation and the fluids inside the stria vascularis. However, the mechanisms that control the permeability of the intrastrial fluid-blood barrier remain largely unknown. The barrier comprises endothelial cells connected to each other by tight junctions and an underlying basement membrane. In a recent study, we found that the intrastrial fluid-blood barrier also includes a large number of perivascular cells with both macrophage and melanocyte characteristics. The perivascular-resident macrophage-like melanocytes (PVM/Ms) are in close contact with vessels through cytoplasmic processes. Here we demonstrate that PVM/Ms have an important role in maintaining the integrity of the intrastrial fluid-blood barrier and hearing function. Using a cell culture-based in vitro model and a genetically induced PVM/M-depleted animal model, we show that absence of PVM/Ms increases the permeability of the intrastrial fluid-blood barrier to both low- and high-molecular-weight tracers. The increased permeability is caused by decreased expression of pigment epithelial-derived factor, which regulates expression of several tight junction-associated proteins instrumental to barrier integrity. When tested for endocochlear potential and auditory brainstem response, PVM/M-depleted animals show substantial drop in endocochlear potential with accompanying hearing loss. Our results demonstrate a critical role for PVM/Ms in regulating the permeability of the intrastrial fluid-blood barrier for establishing a normal endocochlear potential hearing threshold.

  • 102.
    Zhang, Yin
    et al.
    Karolinska Institute, Sweden; Shandong University, Peoples R China; Shandong University, Peoples R China.
    Yang, Yunlong
    Karolinska Institute, Sweden.
    Hosaka, Kayoko
    Karolinska Institute, Sweden.
    Huang, Guichun
    Karolinska Institute, Sweden.
    Zang, Jingwu
    BioSciKin Biopharma, Peoples R China.
    Chen, Fang
    Zhejiang Chinese Medical University, Peoples R China.
    Zhang, Yun
    Karolinska Institute, Sweden; Shandong University, Peoples R China; Shandong University, Peoples R China.
    Samani, Nilesh J.
    University of Leicester, England; Glenfield Gen Hospital, England.
    Cao, Yihai
    Linköpings universitet, Medicinska fakulteten. Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Karolinska Institute, Sweden; University of Leicester, England; Glenfield Gen Hospital, England; Second Hospital Wuxi, Peoples R China.
    Endocrine vasculatures are preferable targets of an antitumor ineffective low dose of anti-VEGF therapy2016Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 113, nr 15, s. 4158-4163Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Anti-VEGF-based antiangiogenic drugs are designed to block tumor angiogenesis for treatment of cancer patients. However, anti-VEGF drugs produce off-tumor target effects on multiple tissues and organs and cause broad adverse effects. Here, we show that vasculatures in endocrine organs were more sensitive to anti-VEGF treatment than tumor vasculatures. In thyroid, adrenal glands, and pancreatic islets, systemic treatment with low doses of an anti-VEGF neutralizing antibody caused marked vascular regression, whereas tumor vessels remained unaffected. Additionally, a low dose of VEGF blockade significantly inhibited the formation of thyroid vascular fenestrae, leaving tumor vascular structures unchanged. Along with vascular structural changes, the low dose of VEGF blockade inhibited vascular perfusion and permeability in thyroid, but not in tumors. Prolonged treatment with the low-dose VEGF blockade caused hypertension and significantly decreased circulating levels of thyroid hormone free-T3 and -T4, leading to functional impairment of thyroid. These findings show that the fenestrated microvasculatures in endocrine organs are more sensitive than tumor vasculatures in response to systemic anti-VEGF drugs. Thus, our data support the notion that clinically nonbeneficial treatments with anti-VEGF drugs could potentially cause adverse effects.

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