Microvilli are microscopic, finger-like extensions of a cell’s plasma membrane that project outward into the surrounding environment. These protrusions are fundamental structures designed to maximize the cell’s ability to interact with the external space. They achieve this by dramatically increasing the functional surface area without significantly increasing the cell’s volume. This adaptation is necessary for processes that require rapid and extensive exchange of materials.
Defining the Architecture of Microvilli
Microvilli are permanent, highly organized extensions of the cell surface, covered by the plasma membrane. Each microvillus is a slender, cylindrical shape, typically measuring about 0.1 micrometers in diameter and 1 to 2 micrometers in length. This uniform size is maintained by a dense, internal core of parallel-running actin filaments.
The structural core contains approximately 20 to 30 tightly bundled actin filaments. These filaments run along the entire length of the projection and are cross-linked and stabilized by proteins such as villin and fimbrin, which maintain the precise hexagonal arrangement of the core. The plus ends of the actin filaments are oriented toward the tip of the microvillus. The core extends into a dense network of intermediate filaments and other proteins just beneath the membrane, known as the terminal web, which provides strong stability to the entire structure.
Primary Locations and the Brush Border
Microvilli are most abundant on the apical surface of epithelial cells in organs dedicated to high-volume absorption and reabsorption. The primary location is the small intestine, where they cover the surface of absorptive enterocytes. In this region, a single epithelial cell can possess thousands of microvilli, creating a highly textured surface.
This collective, dense layer gives the cell surface a characteristic fuzzy or striated appearance when viewed under a light microscope. This dense covering is known as the “brush border,” a term describing its resemblance to the bristles of a brush. Microvilli are also prominent on the epithelial cells lining the proximal convoluted tubules of the kidney. Here, they similarly form a brush border that plays a role in filtering and reclaiming substances from the forming urine.
Surface Area Amplification
The main purpose of microvilli is to vastly amplify the functional surface area of the cell membrane exposed to the lumen. In the small intestine, this structural modification can increase the surface area for absorption by an estimated 20 to 25 times compared to a flat surface. This enormous increase is necessary for the rapid and efficient uptake of digested nutrients from food.
This amplified surface is an active functional layer, not a passive structure. The microvillar membrane is densely packed with specialized digestive enzymes, such as glycosidases, that perform the final breakdown of complex nutrients into smaller, absorbable units. The membrane is also studded with various transport proteins, channels, and pumps. These transporters facilitate the movement of substances like glucose, amino acids, water, and ions across the cell barrier and into the bloodstream. In the kidney, this same principle of surface area amplification, sometimes up to 36-fold in parts of the tubule, enables the efficient reabsorption of essential molecules and water back into the body from the filtrate.
When Microvilli Fail: Clinical Relevance
Defects or damage to the microvilli structure can lead to severe clinical consequences, primarily involving malabsorption. Celiac disease is a common example where an immune reaction to gluten causes inflammation that damages the intestinal lining. This inflammation leads to the blunting and eventual loss of the microvilli, a condition often called villous atrophy. The resulting decrease in surface area and loss of embedded enzymes severely reduces the ability to absorb nutrients, leading to symptoms like diarrhea and weight loss.
A much rarer, life-threatening disorder is Microvillous Inclusion Disease (MVID), a congenital condition that manifests in newborns. MVID is caused by genetic defects, often in the MYO5B gene, which is involved in the formation and organization of the microvilli. This defect results in underdeveloped or absent microvilli and the abnormal presence of microvilli-like structures trapped inside the cell. Infants with MVID suffer from intractable, watery diarrhea and severe malabsorption, often requiring lifelong nutritional support through intravenous feeding.