PPARγ Ligands Regulate Noncontractile and Contractile Functions of Airway Smooth Muscle: Implications for Asthma Therapy

Table 1

Effects of PPARγ ligands in mouse OVA models of allergic airways disease.

Strain	Ligand	Inflammation	Remodeling	AHR	Mechanism	References
Balb/C	CGZ	↓ IL-4, IL-5, IL-6, IL-13; ↓ eosinophils	↓ mucus; ↓ collagen; ↓ wall thickness	↓	↓ GATA-3	[25, 94]
Balb/C	CGZ	↓ IFNγ, IL-2, IL-4; ↓ eosinophils	↓ mucus	N.D.		[100]
Balb/C	CGZ	↓ eosinophils	↓ ASM thickness	↓		[95]
Balb/C	CGZ RGZ	↓ eosinophils		N.D.	↑ IL-10	[99]
Balb/C	RGZ PGZ	↓ IL-4, IL-5, IL-13, ECP; ↓ eosinophils		↓	↑ PTEN; ↑ IL-10	[27, 47]
Balb/C	GI 262570	↓ eosinophils		N.D.		[92]
C57Bl/6	RGZ PGZ	↓ IL-4, IL-5, IL-13,; ↓ VEGF, eotaxin, RANTES; ↓ eosinophils		↓	↑ IL-17 via NF𝜅B	[93, 97]
C57Bl/6	RGZ	⇔ eosinophils	⇔ mucus; ⇔ wall thickness	↓		[98]

ASM: airway smooth muscle; CGZ: ciglitazone; ECP: eosinophil cationic protein; IL: interleukin; N.D.: not determined; PGZ: pioglitazone; PTEN: phosphatase and tensin homologue deleted on chromosome ten; RANTES: regulated upon activation, normal T-cell expressed, and secreted; RGZ: rosiglitazone; VEGF: vascular endothelial growth factor.