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Table 1 Role of dopamine and its receptor on mesenchymal stromal cells and neuron, hematopoietic, cancer stem cells

From: Effects of Dopamine on stem cells and its potential roles in the treatment of inflammatory disorders: a narrative review

Cell type

Classification

Receptors

Signaling pathway

Outcomes

Neural stem cells

 

D2

D2R(+)-cAMP(−)-CNTF(+)-JAK/STAT/Notch1(+)

Promotion of the proliferation and differentiation of neural stem cells

D3

D3R(+)-AKT/ERK1/2(+)

 

D3

D3R(+)-Cdk5/p35(+)

Protection against the loss of nestin expression caused by various stressors to reduce neural stem cell death

Mesenchymal Stromal cells (MSCs)

Human-derived mesenchymal progenitor cells

(hMPCs)

D2

D2R(+)-AKT(+)

Increased mobilization and migration capacity of hMPCs

Murine-derived mesenchymal progenitor cells

(mMPCs)

D2

D2R(+)-VEGFR-2/AKT-VEGF(−)

Reduction of the number of mMSCs and inhibited their ability to mobilization and migration

D2R(+)-AKT(+)

Increased mobilization and migration capacity of mMPCs

Human bone marrow mesenchymal stromal cells

(hBMSCs)

D1/D2

Unknown

A low concentration of dopamine (50 μM) can promote the proliferation and differentiation of hBMSCs, while the high concentration of dopamine (500 μM) can inhibit

D1

D1R(+)-ERK1/2(+)-RUNX2

Low concentrations of dopamine (below 5 nM) can promote osteogenic differentiation of hBMSCs, while high concentrations (above 5 μM) can inhibit

Rat bone marrow mesenchymal stromal cells

(rBMSCs)

Unknown

cAMP-CREB-Ca2+

Affects osteogenic differentiation of rBMSCs

AKT/GSK-3β/β-Catenin

Reduction of osteogenic differentiation of rBMSCs and promoted their lipogenic differentiation

Hematopoietic stem and progenitor cells (HSPCs)

 

D2/D3

D2R/D3R(+)-cAMP(+)-PKA(+)-LCK(+)-c-kit/ERK(+)

Regulation of HSPCs maintenance and enhance their ability to proliferate and differentiate

Cancer stem cells

 

D2

D2R(−)-Wnt/β-catenin(−)

D2 receptor antagonists aripiprazole and methoprazine can inhibit the growth of cancer stem cells and induce apoptosis

 

D2R(−)-AKT(−)

While promoting the differentiation of cancer stem cells into non-cancer cells

Pituitary adenoma stem cells

D2

D2R(+)-PRL(−)

Reduction of the proliferation rate and activity of pituitary tumor stem cells

Glioblastoma neural stem cells

(GNS)

D4

D4R(−)-PDGFRβ(−)-ERK1/2(−)

Inhibition of GNS self-renewal and glioblastoma growth

Breast cancer stem cells

D1

D1R(+)

D1 receptor agonists fenoldopam and L-SPD can inhibit the growth of mouse breast cancer stem cells

  1. L-SPD: L-Stepholidine