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Pietilä, I., van Mourik, D., Tamelander, A., Kriz, V., Claesson-Welsh, L., Tengholm, A. & Welsh, M. (2019). Temporal Dynamics of VEGFA-Induced VEGFR2/FAK Co-Localization Depend on SHB. Cells, 8, Article ID 1645.
Open this publication in new window or tab >>Temporal Dynamics of VEGFA-Induced VEGFR2/FAK Co-Localization Depend on SHB
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2019 (English)In: Cells, ISSN 2073-4409, Vol. 8, article id 1645Article in journal (Refereed) Published
Abstract [en]

Focal adhesion kinase (FAK) is essential for vascular endothelial growth factor-A (VEGFA)/VEGF receptor-2 (VEGFR2)-stimulated angiogenesis and vascular permeability. We have previously noted that presence of the Src homology-2 domain adapter protein B (SHB) is of relevance for VEGFA-stimulated angiogenesis in a FAK-dependent manner. The current study was conducted in order address the temporal dynamics of co-localization between these components in HEK293 and primary lung endothelial cells (EC) by total internal reflection fluorescence microscopy (TIRF). An early (<2.5 min) VEGFA-induced increase in VEGFR2 co-localization with SHB was dependent on tyrosine 1175 in VEGFR2. VEGFA also enhanced SHB co-localization with FAK. FAK co-localization with VEGFR2 was dependent on SHB since it was significantly lower in SHB deficient EC after VEGFA addition. Absence of SHB also resulted in a gradual decline of VEGFR2 co-localization with FAK under basal (prior to VEGFA addition) conditions. A similar basal response was observed with expression of the Y1175F-VEGFR2 mutant in wild type EC. The distribution of focal adhesions in SHB-deficient EC was altered with a primarily perinuclear location. These live cell data implicate SHB as a key component regulating FAK activity in response to VEGFA/VEGFR2.

Place, publisher, year, edition, pages
Basel, Switzerland: MDPI, 2019
Keywords
VEGFR2; FAK; SHB; TIRF; focal adhesions; angiogenesis
National Category
Basic Medicine
Research subject
Molecular Cellbiology
Identifiers
urn:nbn:se:uu:diva-400532 (URN)10.3390/cells8121645 (DOI)
Available from: 2019-12-23 Created: 2019-12-23 Last updated: 2020-01-03Bibliographically approved
He, Q., Li, X., Singh, K., Luo, Z., Meija-Cordova, M., Jamalpour, M., . . . Welsh, M. (2019). The Cdh5-CreERT2 transgene causes conditional Shb gene deletion in hematopoietic cells with consequences for immune cell responses to tumors. Scientific Reports, 9, Article ID 7548.
Open this publication in new window or tab >>The Cdh5-CreERT2 transgene causes conditional Shb gene deletion in hematopoietic cells with consequences for immune cell responses to tumors
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2019 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 9, article id 7548Article in journal (Refereed) Published
Abstract [en]

The tamoxifen-responsive conditional Cdh5-CreERT2 is commonly used for endothelial cell specific conditional deletion of loxP-flanked gene sequences. To address the role of endothelial cell Shb gene for B16F10 melanoma immune responses, tamoxifen-injected Cdh5-CreERT2/WT and Cdh5-CreERT2/Shbflox/flox mice received subcutaneous tumor cell injections. We observed a decrease of tumor myeloid cell Shb mRNA in the tamoxifen treated Cdh5-CreERT2/Shbflox/flox mice, which was not present when the mice had undergone a preceding bone marrow transplantation using wild type bone marrow. Differences in CD4+/FoxP3+ Tregs were similarly abolished by a preceding bone marrow transplantation. In ROSA26-mTmG mice, Cdh5-CreERT2 caused detectable floxing in certain bone marrow populations and in spleen cells. Floxing in bone marrow could be detected two months after tamoxifen treatment. In the spleen, however, floxing was undetectable two months after tamoxifen treatment, suggesting that Cdh5-CreERT2 is operating in a non-renewable population of hematopoietic cells in this organ. These data suggest that conditional gene deletion in hematopoietic cells is a potential confounder in experiments attempting to assess the role of endothelial specific effects. A cautious approach to achieve an endothelial-specific phenotype would be to adopt a strategy that includes a preceding bone marrow transplantation.

National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-383581 (URN)10.1038/s41598-019-44039-z (DOI)000468171100043 ()31101877 (PubMedID)
Funder
Swedish Cancer Society, 180767Swedish Research Council, 2016-01085EU, FP7, Seventh Framework Programme, 312325EXODIAB - Excellence of Diabetes Research in SwedenErnfors Foundation
Available from: 2019-05-17 Created: 2019-05-17 Last updated: 2019-06-24Bibliographically approved
Jamalpour, M., Li, X., Gustafsson, K., Tyner, J. & Welsh, M. (2018). Disparate effects of Shb-gene deficiency on disease characteristics in murine models of myeloid, B-cell and T-cell leukemia. Tumor Biology, 40(4), 1-13
Open this publication in new window or tab >>Disparate effects of Shb-gene deficiency on disease characteristics in murine models of myeloid, B-cell and T-cell leukemia
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2018 (English)In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 40, no 4, p. 1-13Article in journal (Refereed) Published
Abstract [en]

The Src homology-2 domain protein B is an adaptor protein operating downstream of tyrosine kinases. The Shb gene knockout has been found to accelerate p210 Breakpoint cluster region-cAbl oncogene 1 tyrosine kinase-induced leukemia. In human myeloid leukemia were tumors with high Src homology-2 domain protein B mRNA content, tumors were, however, associated with decreased latency and myeloid leukemia exhibiting immune cell characteristics. Thus, the aim of this study was to investigate the effects of Shb knockout on the development of leukemia in three additional models, that is, colony stimulating factor 3 receptor-T618I–induced neutrophilic leukemia, p190 Breakpoint cluster region-cAbl oncogene 1 tyrosine kinase-induced B-cell leukemia, and G12D-Kras-induced T-cell leukemia/thymic lymphoma. Wild-type or Shb knockout bone marrow cells expressing the oncogenes were transplanted to bone marrow–deficient recipients. Organs from moribund mice were collected and further analyzed. Shb knockout increased the development of CSF3RT618I-induced leukemia and increased the white blood cell count at the time of death. In the p190 Breakpoint cluster region-cAbl oncogene 1 tyrosine kinase B-cell model, Shb knockout reduced white blood cell counts without affecting latency, whereas in the G12D-Kras T-cell model, thymus size was increased without major effects on latency, suggesting that Shb knockout accelerates the development thymic lymphoma. Cytokine secretion plays a role in the progression of leukemia, and consequently Shb knockout bone marrows exhibited lower expression of granulocyte colony stimulating factor and interleukin 6 in the neutrophilic model and interleukin 7 and chemokine C-X-C motif ligand 12 (C-X-C motif chemokine 12) in the B-cell model. It is concluded that in experimental mouse models, the absence of the Shb gene exacerbates the disease in myeloid leukemia, whereas it alters the disease characteristics without affecting latency in B- and T-cell leukemia. The results suggest a role of Shb in modulating the disease characteristics depending on the oncogenic insult operating on hematopoietic cells. These findings help explain the outcome of human disease in relation to Src homology-2 domain protein B mRNA content.

Keywords
Myeloid leukemia, lymphocytic/lymphoblastic leukemia, Src homology-2 domain protein B, signal transduction, cytokines
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-347128 (URN)10.1177/1010428318771472 (DOI)29792386 (PubMedID)
Available from: 2018-03-26 Created: 2018-03-26 Last updated: 2019-12-17Bibliographically approved
Roche, F. P., Pietilä, I., Kaito, H., Sjöström, E. O., Sobotzki, N., Noguer, O., . . . Claesson-Welsh, L. (2018). Leukocyte differentiation by histidine-rich glycoprotein/stanniocalcin-2 complex regulates murine glioma growth through modulation of anti-tumor immunity. Molecular Cancer Therapeutics, 17(9), 1961-1972
Open this publication in new window or tab >>Leukocyte differentiation by histidine-rich glycoprotein/stanniocalcin-2 complex regulates murine glioma growth through modulation of anti-tumor immunity
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2018 (English)In: Molecular Cancer Therapeutics, ISSN 1535-7163, E-ISSN 1538-8514, Vol. 17, no 9, p. 1961-1972Article in journal (Refereed) Published
Abstract [en]

The plasma-protein histidine-rich glycoprotein (HRG) is implicated in phenotypic switching of tumor-associated macrophages, regulating cytokine production and phagocytotic activity, thereby promoting vessel normalization and anti-tumor immune responses. To assess the therapeutic effect of HRG gene delivery on CNS tumors, we used adenovirus-encoded HRG to treat mouse intracranial GL261 glioma. Delivery of Ad5-HRG to the tumor site resulted in a significant reduction in glioma growth, associated with increased vessel perfusion and increased CD45+ leukocyte and CD8+ T cell accumulation in the tumor. Antibody-mediated neutralization of colony-stimulating factor-1 suppressed the effects of HRG on CD45+ and CD8+ infiltration. Using a novel protein interaction-decoding technology, TRICEPS-based ligand receptor capture (LRC), we identified Stanniocalcin-2 (STC2) as an interacting partner of HRG on the surface of inflammatory cells in vitro and co-localization of HRG and STC2 in gliomas. HRG reduced the suppressive effects of STC2 on monocyte CD14+ differentiation and STC2-regulated immune response pathways. In consequence, Ad5-HRG treated gliomas displayed decreased numbers of Interleukin-35+ Treg cells, providing a mechanistic rationale for the reduction in GL261 growth in response to Ad5-HRG delivery. We conclude that HRG suppresses glioma growth by modulating tumor inflammation through monocyte infiltration and differentiation. Moreover, HRG acts to balance the regulatory effects of its partner, STC2, on inflammation and innate and/or acquired immunity. HRG gene delivery therefore offers a potential therapeutic strategy to control anti-tumor immunity.

National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:uu:diva-356836 (URN)10.1158/1535-7163.MCT-18-0097 (DOI)000444041300015 ()29945872 (PubMedID)
Funder
Swedish Cancer Society, 16 0585Swedish Cancer Society, 16 0520Swedish Research Council, 2015-02375_3Swedish Research Council, 2016-01085
Note

I. Pietilä and H. Kaito contributed equally to this article.

Available from: 2018-08-08 Created: 2018-08-08 Last updated: 2018-11-26Bibliographically approved
Li, X., Singh, K., Luo, Z., Mejia Cordova, M., Jamalpour, M., Lindahl, B., . . . Welsh, M. (2018). Pro-tumoral immune cell alterations in wild type and Shb-deficient mice in response to 4T1 breast carcinomas. OncoTarget, 9(27), 18720-18733
Open this publication in new window or tab >>Pro-tumoral immune cell alterations in wild type and Shb-deficient mice in response to 4T1 breast carcinomas
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2018 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 9, no 27, p. 18720-18733Article in journal (Refereed) Published
Abstract [en]

To assess mechanisms responsible for breast carcinoma metastasis, 4T1 breast carcinomas were grown orthotopically in wild type or Shb knockout mice. Tumor growth, metastasis, vascular characteristics and immune cell properties were analyzed. Absence of Shb did not affect tumor growth although it increased lung metastasis. Shb knockout mouse tumors showed decreased redness and less developed vascular plexa located at the periphery of the tumors. No difference in overall tumor vascular density, leakage or pericyte coverage was noted between the genotypes although the average vessel size was smaller in the knockout. Tumors induced an increase of CD11b+ cells in spleen, lymph node, thymus, bone marrow and blood. Numbers of Shb knockout CD11b/CD8+ cells were decreased in lymph nodes and bone marrow of tumor bearing mice. Mice with tumors had reduced numbers of CD4+ lymphocytes in blood/lymphoid organs, whereas in most of these locations the proportion of CD4+ cells co-expressing FoxP3 was increased, suggesting a relative increase in Treg cells. This finding was reinforced by increased blood interleukin-35 (IL-35) in wild type tumor bearing mice. Shb knockout blood showed in addition an increased proportion of IL-35 expressing Treg cells, supporting the notion that absence of Shb further promotes tumor evasion from immune cell recognition. This could explain the increased number of lung metastases observed under these conditions. In conclusion, 4T1 tumors alter immune cell responses that promote tumor expansion, metastasis and escape from T cell recognition in an Shb dependent manner. 

National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-347019 (URN)10.18632/oncotarget.24643 (DOI)
Available from: 2018-03-23 Created: 2018-03-23 Last updated: 2018-04-12Bibliographically approved
Jamalpour, M., Li, X., Cavelier, L., Gustafsson, K., Mostoslavsky, G., Höglund, M. & Welsh, M. (2017). Tumor SHB gene expression affects disease characteristics in human acute myeloid leukemia. Tumor Biology, 39(10)
Open this publication in new window or tab >>Tumor SHB gene expression affects disease characteristics in human acute myeloid leukemia
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2017 (English)In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 39, no 10Article in journal (Refereed) Published
Abstract [en]

Objective: The mouse Shb gene coding for the Src Homology 2-domain containing adapter protein B has recently been placed in context of BCRABL1-induced myeloid leukemia in mice and the current study was performed in order to relate SHB to human acute myeloid leukemia (AML). Methods: Publicly available AML databases were mined for SHB gene expression and patient survival. SHB gene expression was determined in the Uppsala cohort of AML patients by qPCR. Cell proliferation was determined after SHB gene knockdown in leukemic cell lines. Results: Despite a low frequency of SHB gene mutations, many tumors overexpressed SHB mRNA compared with normal myeloid blood cells. AML patients with tumors expressing low SHB mRNA displayed longer survival times. A subgroup of AML exhibiting a favorable prognosis, acute promyelocytic leukemia (APL) with a PMLRARA translocation, expressed less SHB mRNA than AML tumors in general. When examining genes co-expressed with SHB in AML tumors, four other genes (PAX5, HDAC7, BCORL1, TET1) related to leukemia were identified. A network consisting of these genes plus SHB was identified that relates to certain phenotypic characteristics, such as immune cell, vascular and apoptotic features. SHB knockdown in the APL PMLRARA cell line NB4 and the monocyte/macrophage cell line MM6 adversely affected proliferation, linking SHB gene expression to tumor cell expansion and consequently to patient survival. Conclusions: It is concluded that tumor SHB gene expression relates to AML survival and its subgroup APL. Moreover, this gene is included in a network of genes that plays a role for an AML phenotype exhibiting certain immune cell, vascular and apoptotic characteristics.

National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-330892 (URN)10.1177/1010428317720643 (DOI)
Funder
Swedish Cancer SocietySwedish Research Council
Available from: 2017-10-06 Created: 2017-10-06 Last updated: 2018-01-13Bibliographically approved
Jamalpour, M., Li, X., Cavelier, L., Gustafsson, K., Mostoslavsky, G., Höglund, M. & Welsh, M. (2017). Tumor SHB gene expression affects disease characteristics in human acute myeloid leukemia. Tumor Biology, 39(10), Article ID 1010428317720643.
Open this publication in new window or tab >>Tumor SHB gene expression affects disease characteristics in human acute myeloid leukemia
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2017 (English)In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 39, no 10, article id 1010428317720643Article in journal (Refereed) Published
Abstract [en]

The mouse Shb gene coding for the Src Homology 2-domain containing adapter protein B has recently been placed in context of BCRABL1-induced myeloid leukemia in mice and the current study was performed in order to relate SHB to human acute myeloid leukemia (AML). Publicly available AML databases were mined for SHB gene expression and patient survival. SHB gene expression was determined in the Uppsala cohort of AML patients by qPCR. Cell proliferation was determined after SHB gene knockdown in leukemic cell lines. Despite a low frequency of SHB gene mutations, many tumors overexpressed SHB mRNA compared with normal myeloid blood cells. AML patients with tumors expressing low SHB mRNA displayed longer survival times. A subgroup of AML exhibiting a favorable prognosis, acute promyelocytic leukemia (APL) with a PMLRARA translocation, expressed less SHB mRNA than AML tumors in general. When examining genes co-expressed with SHB in AML tumors, four other genes (PAX5, HDAC7, BCORL1, TET1) related to leukemia were identified. A network consisting of these genes plus SHB was identified that relates to certain phenotypic characteristics, such as immune cell, vascular and apoptotic features. SHB knockdown in the APL PMLRARA cell line NB4 and the monocyte/macrophage cell line MM6 adversely affected proliferation, linking SHB gene expression to tumor cell expansion and consequently to patient survival. It is concluded that tumor SHB gene expression relates to AML survival and its subgroup APL. Moreover, this gene is included in a network of genes that plays a role for an AML phenotype exhibiting certain immune cell, vascular and apoptotic characteristics.

Keywords
Acute myeloid leukemia, acute promyelocytic leukemia, immune cell, angiogenesis, SHB/PAX5/HDAC7/BCORL1/TET1 network
National Category
Basic Medicine Cancer and Oncology
Research subject
Oncology
Identifiers
urn:nbn:se:uu:diva-400533 (URN)10.1177/1010428317720643 (DOI)28982308 (PubMedID)
Funder
Swedish Cancer SocietyErnfors FoundationSwedish Research CouncilEXODIAB - Excellence of Diabetes Research in Sweden
Available from: 2019-12-23 Created: 2019-12-23 Last updated: 2020-01-09Bibliographically approved
Welsh, M. (2016). Claes Hellerström and Cartesian Diver respirometry. Upsala Journal of Medical Sciences, 121(2), 77-80
Open this publication in new window or tab >>Claes Hellerström and Cartesian Diver respirometry
2016 (English)In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 121, no 2, p. 77-80Article in journal (Refereed) Published
Abstract [en]

Cartesian diver microrespirometry was introduced by Claes Hellerström at the Department of Histology/Medical Cell Biology at Uppsala University, Sweden, to determine rates of oxygen consumption in islets of Langerhans. The theory behind this method is touched upon and the main findings described. Glucose-stimulated beta cell respiration significantly contributes to increased ATP generation, which is a prerequisite for stimulated insulin secretion and synthesis. This has had major implications for understanding the beta cell stimulus secretion coupling.

Keywords
Cartesian diver; glucose; insulin secretion; islets of Langerhans; respiration
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:uu:diva-269505 (URN)10.3109/03009734.2015.1109012 (DOI)000376695600003 ()27181825 (PubMedID)
Funder
Swedish Diabetes Association
Available from: 2015-12-16 Created: 2015-12-16 Last updated: 2018-01-10Bibliographically approved
Massena, S., Christoffersson, G., Vågesjö, E., Seignez, C., Gustafsson, K., Binet, F., . . . Phillipson, M. (2015). Identification and characterization of VEGF-A-responsive neutrophils expressing CD49d, VEGFR1, and CXCR4 in mice and humans. Blood, 126(17), 2016-2026
Open this publication in new window or tab >>Identification and characterization of VEGF-A-responsive neutrophils expressing CD49d, VEGFR1, and CXCR4 in mice and humans
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2015 (English)In: Blood, ISSN 0006-4971, E-ISSN 1528-0020, Vol. 126, no 17, p. 2016-2026Article in journal (Refereed) Published
Abstract [en]

Vascular endothelial growth factor A (VEGF-A) is upregulated during hypoxia and is the major regulator of angiogenesis. VEGF-A expression has also been found to recruit myeloid cells to ischemic tissues where they contribute to angiogenesis. This study investigates the mechanisms underlying neutrophil recruitment to VEGF-A as well as the characteristics of these neutrophils. A previously undefined circulating subset of neutrophils shown to be CD49d(+)VEGFR1(high)CXCR4(high) was identified in mice and humans. By using chimeric mice with impaired VEGF receptor 1 (VEGFR1) or VEGFR2 signaling (Flt-1tk(-/-), tsad(-/-)), we found that parallel activation of VEGFR1 on neutrophils and VEGFR2 on endothelial cells was required for VEGF-A-induced recruitment of circulating neutrophils to tissue. Intravital microscopy of mouse microcirculation revealed that neutrophil recruitment by VEGF-A versus by the chemokine macrophage inflammatory protein 2 (MIP-2 [CXCL2]) involved the same steps of the recruitment cascade but that an additional neutrophil integrin (eg, VLA-4 [CD49d/CD29]) played a crucial role in neutrophil crawling and emigration to VEGF-A. Isolated CD49d(+) neutrophils featured increased chemokinesis but not chemotaxis compared with CD49d(-) neutrophils in the presence of VEGF-A. Finally, by targeting the integrin α4 subunit (CD49d) in a transplantation-based angiogenesis model that used avascular pancreatic islets transplanted to striated muscle, we demonstrated that inhibiting the recruitment of circulating proangiogenic neutrophils to hypoxic tissue impairs vessel neoformation. Thus, angiogenesis can be modulated by targeting cell-surface receptors specifically involved in VEGF-A-dependent recruitment of proangiogenic neutrophils without compromising recruitment of the neutrophil population involved in the immune response to pathogens.

National Category
Physiology
Identifiers
urn:nbn:se:uu:diva-265201 (URN)10.1182/blood-2015-03-631572 (DOI)000366389200012 ()26286848 (PubMedID)
Funder
Swedish Research CouncilThe Royal Swedish Academy of SciencesMagnus Bergvall FoundationSwedish Diabetes AssociationÅke Wiberg FoundationRagnar Söderbergs stiftelseKnut and Alice Wallenberg Foundation
Available from: 2015-10-25 Created: 2015-10-25 Last updated: 2018-01-10Bibliographically approved
Nikpour, M., Gustafsson, K., Vågesjö, E., Seignez, C., Giraud, A., Phillipson, M. & Welsh, M. (2015). Shb deficiency in endothelium but not in leukocytes is responsible for impaired vascular performance during hindlimb ischemia.. Acta Physiologica, 214(2), 200-209
Open this publication in new window or tab >>Shb deficiency in endothelium but not in leukocytes is responsible for impaired vascular performance during hindlimb ischemia.
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2015 (English)In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 214, no 2, p. 200-209Article in journal (Refereed) Published
Abstract [en]

Aim: Myeloid cells have been suggested to participate in angiogenesis and regulation of vascular function. Shb-deficient mice display both vascular and myeloid cell abnormalities with possible consequences for recovery after hindlimb ischemia. This study was conducted in order to assess the contribution of Shb-deficiency in myeloid cells to impaired vascular function in ischemia. Methods: Wild type and Shb-deficient mice were subjected to peritoneal VEGFA followed by intraperitoneal lavage, after which blood and peritoneal cells were stained for myeloid markers. VEGFA-induced leukocyte recruitment to cremaster muscle was investigated using intravital microscopy of both mouse strains. Blood flow after femoral artery ligation was determined on chimeric mice after bone marrow transplantation. Results: No differences in neutrophil numbers or cell surface phenotypes were detected. Moreover, neutrophil extravasation in VEGFA-activated cremaster muscle was unaffected by Shb deficiency. However, blood and peritoneal CXCR4+ monocytes/macrophages were reduced in response to intraperitoneal VEGFA but not LPS in the absence of Shb. Furthermore, the macrophage population in ischemic muscle was unaffected by Shb-deficiency after two days but reduced seven days after injury. The bone marrow transplantation experiments revealed that mice with wild type vasculature showed better blood flow than those with Shb-deficient vasculature irrespective of leukocyte genotype. Conclusion: The observed aberrations in myeloid cell properties in Shb-deficient mice are likely consequences of an abnormal vascular compartment and are not responsible for reduced muscle blood flow. Structural vascular abnormalities seem to be the primary cause of poor vascular performance under provoked vascular stress in this genetic model.

National Category
Physiology
Research subject
Medical Cell Biology
Identifiers
urn:nbn:se:uu:diva-240416 (URN)10.1111/apha.12448 (DOI)000354389100009 ()25561022 (PubMedID)
Available from: 2015-01-07 Created: 2015-01-07 Last updated: 2018-01-11Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-5467-9755

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