Monocyte macrophage differentiation in vitro: Fibronectin-dependent upregulation of certain macrophage-specific activities

Sudhakaran, P. R.; Radhika, Achuthan; Jacob, Shiney Susan

doi:10.1007/s10719-006-9011-2

Cited by 36 publications

(25 citation statements)

References 32 publications

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“…Treating HL-60 cells with molecules that upregulate CD11b increases inducible oxidative metabolism [6,49]. Membrane-localized Fgr plays a role in integrin receptor signaling [50], and integrin signaling may be important for hematopoietic myelo-monocytic differentiation [51,52]. This suggests that the compromised induced expression of both Fgr and CD11b may decrease the oxidative metabolism capability in CD38 Δ11–20 cells that is normally characteristic of differentiated myelocytes.…”

Section: Discussionmentioning

confidence: 99%

ATRA-induced HL-60 myeloid leukemia cell differentiation depends on the CD38 cytosolic tail needed for membrane localization, but CD38 enzymatic activity is unnecessary

Congleton

Jiang

Malavasi

et al. 2011

Experimental Cell Research

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Leukocyte antigen CD38 expression is an early marker of all-trans retinoic acid (ATRA) stimulated differentiation in the leukemic cell line HL-60. It promotes induced myeloid maturation when overexpressed, whereas knocking it down is inhibitory. It is a type II membrane protein with an extracellular C-terminal enzymatic domain with NADase/NADPase and ADPR cyclase activity and a short cytoplasmic N-terminal tail. Here we determined whether CD38 enzymatic activity or the cytoplasmic tail is required for ATRA-induced differentiation. Neither a specific CD38 ectoenzyme inhibitor nor a point mutation that cripples enzymatic activity (CD38 E226Q) diminishes ATRA-induced differentiation or G1/0 arrest. In contrast a cytosolic deletion mutation (CD38 Δ11–20) prevents membrane expression and inhibits differentiation and G1/0 arrest. These results may be consistent with disrupting the function of critical molecules necessary for membrane-expressed CD38 signal transduction. One candidate molecule is the Src family kinase Fgr, which failed to undergo ATRA-induced upregulation in CD38 Δ11–20 expressing cells. Another is Vav1, which also showed only basal expression after ATRA treatment in CD38 Δ11–20 expressing cells. Therefore, the ability of CD38 to propel ATRA-induced myeloid differentiation and G1/0 arrest is unimpaired by loss of its ectoenzyme activity. However a cytosolic tail deletion mutation disrupted membrane localization and inhibited differentiation. ATRA-induced differentiation thus does not require the CD38 ectoenzyme function, but is dependent on a membrane receptor function.

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Section: Discussionmentioning

confidence: 99%

ATRA-induced HL-60 myeloid leukemia cell differentiation depends on the CD38 cytosolic tail needed for membrane localization, but CD38 enzymatic activity is unnecessary

Congleton

Jiang

Malavasi

et al. 2011

Experimental Cell Research

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“…These proteins aid in monocyte adhesion to components of extracellular matrices and are central to inflammation, immunity, and homeostasis [24]. The adhesive properties of integrins contribute to different patterns of monocyte differentiation under various conditions [21], [22], [25].…”

Section: Introductionmentioning

confidence: 99%

NaCl Potentiates Human Fibrocyte Differentiation

2012

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Excessive NaCl intake is associated with a variety of fibrosing diseases such as renal and cardiac fibrosis. This association has been attributed to increased blood pressure as the result of high NaCl intake. However, studies in patients with high NaCl intake and fibrosis reveal a connection between NaCl intake and fibrosis that is independent of blood pressure. We find that increasing the extracellular concentration of NaCl to levels that may occur in human blood after high-salt intake can potentiate, in serum-free culture conditions, the differentiation of freshly-isolated human monocytes into fibroblast-like cells called fibrocytes. NaCl affects the monocytes directly during their adhesion. Potassium chloride and sodium nitrate also potentiate fibrocyte differentiation. The plasma protein Serum Amyloid P (SAP) inhibits fibrocyte differentiation. High levels of extracellular NaCl change the SAP Hill coefficient from 1.7 to 0.8, and cause a four-fold increase in the concentration of SAP needed to inhibit fibrocyte differentiation by 95%. Together, our data suggest that NaCl potentiates fibrocyte differentiation. NaCl-increased fibrocyte differentiation may thus contribute to NaCl-increased renal and cardiac fibrosis.

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“…Monocyte adhesion to the endothelium initiates changes in their gene expression important in differentiation and extravasation [12]. During diapedesis, monocytes also closely interact with extracellular matrix components, in part through integrin receptor interaction, which can further activate these cells towards macrophage differentiation [15-17]. Integrin-mediated activation of monocytes is characterized by a tyrosine-kinase dependent proinflammatory signaling response and release of multiple proinflammatory molecules [7,18-21].…”

Section: Introductionmentioning

confidence: 99%

Adhesion of monocytes to type I collagen stimulates an APP-dependent proinflammatory signaling response and release of Aβ1-40

Sondag

Combs

2010

J Neuroinflammation

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BackgroundAmyloid precursor protein (APP) is a ubiquitously expressed cell surface protein reported to be involved in mediating cell-cell or cell-matrix interactions. Prior work has demonstrated that APP co-localizes with β1 integrin in different cell types.MethodsIn an effort to determine the function of APP on monocytic lineage cells, in particular, the human monocyte cell line, THP-1, was used to assess the role of APP during adhesion to the extracelluar matrix component type I collagen.ResultsPull-down assays demonstrated that THP-1 adhesion to collagen stimulated a tyrosine kinase-associated signaling response which included subsequent phosphorylation of p38 MAP kinase and increased association of APP with α2β1 integrin, specifically. In addition, cell adhesion was dependent upon APP expression since APP siRNA knockdown attenuated THP-1 adhesion to collagen compared to mock transfected controls. One consequence of the tyrosine kinase-dependent signaling response was increased secretion of interleukin-1β (IL-1β) and Aβ1-40 but not the Aβ1-42 fragment of APP. Increased secretion of IL-1β was dependent upon p38 MAP kinase activity while Aβ1-40 secretion required Src family kinase activity since the specific p38 inhibitor, SB202190, and the Src family kinase inhibitor, PP2, attenuated IL-1β and Aβ1-40 secretion, respectively.ConclusionsThese data demonstrate that APP is involved in classic integrin-dependent tyrosine kinase-associated adhesion and activation of peripheral monocytic cells. Moreover, divergent APP-dependent signaling is required for increased secretion of both IL-1β and Aβ1-40 as a component of the adhesion-dependent change in phenotype. This suggests that APP may have a broad role in not only mediating cell-matrix adhesion but also in the function of peripheral immune cells.

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Monocyte macrophage differentiation in vitro: Fibronectin-dependent upregulation of certain macrophage-specific activities

Cited by 36 publications

References 32 publications

ATRA-induced HL-60 myeloid leukemia cell differentiation depends on the CD38 cytosolic tail needed for membrane localization, but CD38 enzymatic activity is unnecessary

ATRA-induced HL-60 myeloid leukemia cell differentiation depends on the CD38 cytosolic tail needed for membrane localization, but CD38 enzymatic activity is unnecessary

NaCl Potentiates Human Fibrocyte Differentiation

Adhesion of monocytes to type I collagen stimulates an APP-dependent proinflammatory signaling response and release of Aβ1-40

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