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Arrestin Beta 2

The Experts below are selected from a list of 12 Experts worldwide ranked by ideXlab platform

Veronika Grau – 1st expert on this subject based on the ideXlab platform

  • reduced expression of Arrestin Beta 2 by graft monocytes during acute rejection of rat kidneys
    Immunobiology, 2011
    Co-Authors: Anna Zakrzewicz, Gabriela Krasteva, Jochen Wilhelm, Hartmut Dietrich, Sigrid Wilker, W Padberg, Malgorzata Wygrecka, Veronika Grau

    Abstract:

    During acute rejection, numerous pro-inflammatory and cytotoxic monocytes accumulate in the vasculature of experimental renal allografts. Arrestins (ARRBs) are cellular regulators of inflammation, but nothing is known about their expression during rejection. Intravascular mononuclear graft leukocytes were isolated 4 days after kidney transplantation. ARRB1 and ARRB2 mRNA expression was reduced in blood leukocytes from allografts undergoing acute rejection, whereas on the protein level only ARRB2 was changed. Flow cytometry and confocal microscopy revealed ARRB1 and ARRB2 expression by monocytes and T cells, with a selective decrease in ARRB2 expression in monocytes during acute rejection. I-κB directly interacted with ARRB2 and the levels of both proteins strongly correlated. Concomitantly, the mRNA expression of NF-κB targeted genes increased. Our results suggest that activation of blood monocytes in renal isografts is dampened by high ARRB2 levels. During acute rejection, ARRB2 levels are reduced and classical monocyte activation is enabled via NF-κB activation.

Anna Zakrzewicz – 2nd expert on this subject based on the ideXlab platform

  • reduced expression of Arrestin Beta 2 by graft monocytes during acute rejection of rat kidneys
    Immunobiology, 2011
    Co-Authors: Anna Zakrzewicz, Gabriela Krasteva, Jochen Wilhelm, Hartmut Dietrich, Sigrid Wilker, W Padberg, Malgorzata Wygrecka, Veronika Grau

    Abstract:

    During acute rejection, numerous pro-inflammatory and cytotoxic monocytes accumulate in the vasculature of experimental renal allografts. Arrestins (ARRBs) are cellular regulators of inflammation, but nothing is known about their expression during rejection. Intravascular mononuclear graft leukocytes were isolated 4 days after kidney transplantation. ARRB1 and ARRB2 mRNA expression was reduced in blood leukocytes from allografts undergoing acute rejection, whereas on the protein level only ARRB2 was changed. Flow cytometry and confocal microscopy revealed ARRB1 and ARRB2 expression by monocytes and T cells, with a selective decrease in ARRB2 expression in monocytes during acute rejection. I-κB directly interacted with ARRB2 and the levels of both proteins strongly correlated. Concomitantly, the mRNA expression of NF-κB targeted genes increased. Our results suggest that activation of blood monocytes in renal isografts is dampened by high ARRB2 levels. During acute rejection, ARRB2 levels are reduced and classical monocyte activation is enabled via NF-κB activation.

Malgorzata Wygrecka – 3rd expert on this subject based on the ideXlab platform

  • reduced expression of Arrestin Beta 2 by graft monocytes during acute rejection of rat kidneys
    Immunobiology, 2011
    Co-Authors: Anna Zakrzewicz, Gabriela Krasteva, Jochen Wilhelm, Hartmut Dietrich, Sigrid Wilker, W Padberg, Malgorzata Wygrecka, Veronika Grau

    Abstract:

    During acute rejection, numerous pro-inflammatory and cytotoxic monocytes accumulate in the vasculature of experimental renal allografts. Arrestins (ARRBs) are cellular regulators of inflammation, but nothing is known about their expression during rejection. Intravascular mononuclear graft leukocytes were isolated 4 days after kidney transplantation. ARRB1 and ARRB2 mRNA expression was reduced in blood leukocytes from allografts undergoing acute rejection, whereas on the protein level only ARRB2 was changed. Flow cytometry and confocal microscopy revealed ARRB1 and ARRB2 expression by monocytes and T cells, with a selective decrease in ARRB2 expression in monocytes during acute rejection. I-κB directly interacted with ARRB2 and the levels of both proteins strongly correlated. Concomitantly, the mRNA expression of NF-κB targeted genes increased. Our results suggest that activation of blood monocytes in renal isografts is dampened by high ARRB2 levels. During acute rejection, ARRB2 levels are reduced and classical monocyte activation is enabled via NF-κB activation.