Table 2.

Skeletal and hematopoietic phenotypes from experimental manipulation of niche cellular populations in vivo.

Cell Population	Experimental Manipulation	Bone Phenotype	Effects on Hematopoiesis	References
CD146+	Subcutaneous transplantation	Ectopic bone formation	Can recruit hematopoietic marrow	[20-22]
CD105+ Thy1.1− 6C3−	Renal capsule transplantation	Ectopic bone formation	Multilineage mesenchymal potential in vitro Can give rise to stromal cells, chondrocytes and osteoblasts in vivo Can recruit hematopoietic marrow	[32, 33]
CD105+ Thy1.1+ 6C3−	Renal capsule transplantation	Ectopic bone formation	Enriched in expression of osteocalcin Cannot recruit hematopoietic marrow	[32, 33]
CD105+ Thy1.1− 6C3+	Renal capsule transplantation	Ectopic bone formation	Contribute to HSC niche	[33]
CD105− Thy1.1+ 6C3−	Co-culture and transplantation of HSCs		Contribute to B lymphocyte niche	[33]
CXCL12+	Ablation by diphtheria toxin	Impaired osteogenic and adipogenic potential of bone marrow cells	Loss of bone marrow CLPs, GMPs, MEPs, pro-B cells and proerythroblasts Reduced frequency of bone marrow HSCs Increased HSC quiescence Increased expression of myeloid genes in HSCs	[37]
Nestin+ mesenchymal progenitors	Subcutaneous transplantation	Ectopic bone formation	Can recruit hematopoietic marrow	[29]
Nestin+ mesenchymal progenitors	Ablation by diphtheria toxin		Loss of bone marrow HSPCs	[29]
Nestin+ mesenchymal progenitors	Deletion of SCF		No loss of bone marrow HSPCs	[31]
Nestin+ mesenchymal progenitors	Deletion of CXCL12		No loss of bone marrow HSPCs	[30]
LepR+ mesenchymal progenitors	Deletion of SCF		Loss of bone marrow HSPCs	[31]
LepR+ mesenchymal progenitors	Deletion of CXCL12		Peripheral mobilization of HSPCs	[30]
Prx1+ mesenchymal progenitors	Deletion of CXCL12		Loss of bone marrow HSPCs, CLPs, prepro-B cells Loss of HSC quiescence Peripheral mobilization of HSPCs	[30, 36]
Osx+ osteoprogenitors	Deletion of Gsα	Reduced trabecular and cortical bone	Arrest in B cell development at pro-B stage	[52]
Osx+ osteoprogenitors	Deletion of CXCL12		Loss of bone marrow CLPs and prepro-B cells Peripheral mobilization of HSPCs	[36]
Osx+ osteoprogenitors	Deletion of VHL	Increased trabecular bone	increase in HSCs and erythroid progenitors Decrease in peripheral blood lymphocytes	[75]
2.3 kb ColI+ osteoblast	Ablation by GCV administration	Reduced trabecular bone	Decrease in B cell precursors, erythroid progenitors Later decline in HSCs	[18]
2.3 kb ColI+ osteoblast	Expression of constitutively active PPR	Increased trabecular bone and peritrabecular stromal cells	Increase in HSCs	[15]
2.3 kb ColI+ osteoblast	Deletion of CXCL12		Loss of CLPs	[30]
2.3 kb ColI+ osteoblast	Deletion of SCF		No hematopoietic phenotype	[31]
2.3 kb ColI+ osteoblast	Expression of constitutively active Gs- coupled 5HT4 serotonin receptor	Increased trabecular bone	Decrease in HSCs Delayed recovery of megakaryocytes and erythroid cells after injury	[55]
Osteocalcin+ osteoblast	Ablation by GCV administration	Increased bone mass and cortical thickness	No hematopoietic phenotype	[19]
Osteocalcin+ osteoblast	Deletion of CXCL12		No hematopoietic phenotype	[36]
Dmp1+ osteocytes	Deletion of Gsα	Osteopenia	Increased neutrophils and platelets Decreased erythroid progenitors	[54]
Dmp1+ osteocytes	Deletion of PPR		No hematopoietic phenotype	[54]
Dmp1+ osteocytes	Expression of constitutively active PPR	Increased trabecular bone but no increase in peritrabecular stromal cells	No change in frequency of HSCs	[50]
Tie2+ endothelial cells	Deletion of SCF		Loss of bone marrow HSPCs	[31]
Tie2+ endothelial cells	Deletion of CXCL12		No hematopoietic phenotype (Greenbaum) Slight reduction in bone marrow HSC frequency (Ding)	[30, 36]